Current Issues in Molecular Biology

Editorial

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Open AccessEditorial

Molecular Biology: Navigating the Landscape

by Madhav Bhatia

Curr. Issues Mol. Biol. 2026, 48(2), 133; https://doi.org/10.3390/cimb48020133 - 26 Jan 2026

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Abstract

“Latest Review Papers in Molecular Biology 2025”, a Special Issue of Current Issues in Molecular Biology (CIMB), was open for publishing review articles on navigating the landscape in molecular biology [...] Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

Review

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27 pages, 1025 KB

Open AccessReview

Botanical Adjuvants in Oncology: A Review on Natural Compounds in Synergy with Conventional Therapies as Next-Generation Enhancers of Breast Cancer Treatment

by Hidaya Mansouri, Ahmed Irchad, Clarence Rubaka, Lydia Kisula, Abdou Azali Hamza and Elingarami Sauli

Curr. Issues Mol. Biol. 2026, 48(2), 170; https://doi.org/10.3390/cimb48020170 - 2 Feb 2026

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Abstract

Breast cancer remains a major global health challenge despite advances in chemotherapy, endocrine therapy, targeted therapy, and radiotherapy, which are frequently constrained by therapeutic resistance, cumulative toxicity, and high costs. Accumulating preclinical and translational evidence demonstrates that plant-derived natural compounds can synergistically enhance [...] Read more.

Breast cancer remains a major global health challenge despite advances in chemotherapy, endocrine therapy, targeted therapy, and radiotherapy, which are frequently constrained by therapeutic resistance, cumulative toxicity, and high costs. Accumulating preclinical and translational evidence demonstrates that plant-derived natural compounds can synergistically enhance the efficacy of conventional treatments, improve tumor response, and potentially reduce adverse effects. This review critically synthesizes in vitro, in vivo, and emerging clinical studies from 2015 to 2025, focusing on key phytochemicals, including curcumin, epigallocatechin-3-gallate, resveratrol, kaempferol, genistein, and other bioactive molecules as stand alone agents and as mechanistically validated adjuvants to chemotherapy, hormonal therapy, and radiotherapy. These compounds exert complementary actions, including the inhibition of PI3K/Akt/mTOR and NF-κB signaling, induction of apoptosis and cell-cycle arrest, suppression of epithelial–mesenchymal transition, and modulation of drug resistance pathways. Preclinical studies consistently show that combination strategies enhance tumor inhibition and may permit cytotoxic dose reduction, mitigating systemic and cardiotoxic effects. Nanocarrier-based delivery systems further optimize solubility, bioavailability, and tumor targeting. Despite robust preclinical evidence, clinical translation is limited by variability in raw materials, lack of standardization, regulatory barriers, and scarce large-scale trials. This review emphasizes both the therapeutic promise and translational challenges of integrating natural compounds as synergistic adjuvants in evidence-based breast cancer therapy. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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29 pages, 733 KB

Open AccessReview

Spermatogenesis Beyond DNA: Integrated RNA Control of the Epitranscriptome and Three-Dimensional Genome Architecture

by Aris Kaltsas, Maria-Anna Kyrgiafini, Zissis Mamuris, Michael Chrisofos and Nikolaos Sofikitis

Curr. Issues Mol. Biol. 2026, 48(1), 123; https://doi.org/10.3390/cimb48010123 - 22 Jan 2026

Cited by 1 | Viewed by 1006

Abstract

Spermatogenesis is a tightly coordinated differentiation program that sustains male fertility while transmitting genetic and epigenetic information to the next generation. This review consolidates mechanistic evidence showing how RNA-centered regulation integrates with the epitranscriptome and three-dimensional (3D) genome architecture to orchestrate germ-cell fate [...] Read more.

Spermatogenesis is a tightly coordinated differentiation program that sustains male fertility while transmitting genetic and epigenetic information to the next generation. This review consolidates mechanistic evidence showing how RNA-centered regulation integrates with the epitranscriptome and three-dimensional (3D) genome architecture to orchestrate germ-cell fate transitions from spermatogonial stem cells through meiosis and spermiogenesis. Recent literature is critically surveyed and synthesized, with particular emphasis on human and primate data and on stage-resolved maps generated by single-cell and multi-omics technologies. Collectively, available studies support a layered regulatory model in which RNA-binding proteins and RNA modifications coordinate transcript processing, storage, translation, and decay; small and long noncoding RNAs shape post-transcriptional programs and transposon defense; and dynamic chromatin remodeling and 3D reconfiguration align transcriptional competence with recombination, sex-chromosome silencing, and genome packaging. Convergent nodes implicated in spermatogenic failure are highlighted, including defects in RNA metabolism, piRNA pathway integrity, epigenetic reprogramming, and nuclear architecture, and the potential of these frameworks to refine molecular phenotyping in male infertility is discussed. Finally, key gaps and priorities for causal testing in spatially informed, stage-specific experimental systems are outlined. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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20 pages, 1101 KB

Open AccessReview

Mediterranean Diet and Oxidative Balance During Pregnancy: Molecular Insights into Mitigating the Impact of Environmental Pollution

by Eirini Kontopidou, Areti Kourti, Apostolos Athanasiadis and Aikaterini Itziou

Curr. Issues Mol. Biol. 2026, 48(1), 115; https://doi.org/10.3390/cimb48010115 - 21 Jan 2026

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Abstract

Pregnancy represents a period of heightened oxidative demand in which maternal metabolic adaptations are tightly regulated by redox-sensitive molecular pathways. Imbalances in these systems have been associated with gestational complications, impaired placental function, and long-term effects on offspring health. This review examines the [...] Read more.

Pregnancy represents a period of heightened oxidative demand in which maternal metabolic adaptations are tightly regulated by redox-sensitive molecular pathways. Imbalances in these systems have been associated with gestational complications, impaired placental function, and long-term effects on offspring health. This review examines the molecular mechanisms through which adherence to the Mediterranean diet (MD) influences oxidative balance during pregnancy. We summarize evidence on how MD-derived bioactives regulate oxidative stress pathways and affect oxidative stress biomarkers, as well as the expression of antioxidant enzymes such as superoxide dismutase and glutathione peroxidase. At the same time, certain MD foods containing environmental contaminants may potentially attenuate its protective effects. In addition, the review explores molecular insights into how the MD may counteract oxidative stress induced by environmental pollutants through modulation of redox signaling and detoxification pathways. By integrating biochemical, molecular, and environmental perspectives, this review highlights the MD as a potential nutrigenomic intervention to optimize oxidative balance, support healthy pregnancy outcomes linked to environmental pollution. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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14 pages, 667 KB

Open AccessReview

Regulatory B Cells in Tumor Microenvironment

by Zhuoyan Cai and Lin Xie

Curr. Issues Mol. Biol. 2026, 48(1), 106; https://doi.org/10.3390/cimb48010106 - 20 Jan 2026

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Abstract

Regulatory B cells (Bregs) are integral to the tumor microenvironment (TME) and influence immune responses through the secretion of immunosuppressive cytokines such as IL-10, IL-35, and TGF-β. This review highlights recent findings on the phenotype and mechanisms of Bregs, emphasizing their dual role [...] Read more.

Regulatory B cells (Bregs) are integral to the tumor microenvironment (TME) and influence immune responses through the secretion of immunosuppressive cytokines such as IL-10, IL-35, and TGF-β. This review highlights recent findings on the phenotype and mechanisms of Bregs, emphasizing their dual role in regulating immune responses within the TME. Importantly, we further explored the latest advances in Breg regulatory mechanisms from the novel perspectives of epigenetics and metabolic remodeling, including the effects of DNA methylation, histone acetylation, glycolysis, and oxidative phosphorylation on Bregs. We also investigate the therapeutic targeting of Bregs, with a focus on STAT3 inhibitors such as lipoxin A4, cucurbitacins, and resveratrol, which show promising potential in mitigating the suppressive function of Bregs. Furthermore, this review provides a detailed analysis of the impact of Bregs on tumorigenesis and metastasis, emphasizing the importance of inhibiting specific immune pathways to prevent tumor escape. Finally, this review offers a prospective outlook on immunotherapy strategies based on Bregs, foreseeing a more nuanced understanding of their TME function and the evolution of targeted treatments with enhanced therapeutic efficacy. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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30 pages, 5371 KB

Open AccessReview

Hypoxia Signaling and Non-Coding RNAs: Regulatory Networks and Therapeutic Implications in Breast Cancer

by Xin Hu, Rui Chen, Famin Ke, Dandan Wang, Xiaowei Gao, Can Song, Aimin Fu, Zuojin Ao, Hanyu Yang, Xiaoyan Liu, Xiurong Guo and Qiuyu Liu

Curr. Issues Mol. Biol. 2026, 48(1), 98; https://doi.org/10.3390/cimb48010098 - 18 Jan 2026

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Abstract

The hypoxic microenvironment within breast cancer tumors leads to the sustained activation of hypoxia-inducible factors (HIFs), notably HIF-1α, which, in turn, triggers adaptive responses such as angiogenesis and metabolic reprogramming. These processes contribute to tumor invasion, progression, metastasis, and therapy resistance. Although a [...] Read more.

The hypoxic microenvironment within breast cancer tumors leads to the sustained activation of hypoxia-inducible factors (HIFs), notably HIF-1α, which, in turn, triggers adaptive responses such as angiogenesis and metabolic reprogramming. These processes contribute to tumor invasion, progression, metastasis, and therapy resistance. Although a substantial portion of the human genome is transcribed into non-coding RNAs (ncRNAs), which have been shown to play key regulatory roles in the development and progression of breast cancer, the interplay between HIFs and ncRNAs—and how such crosstalk influences breast cancer pathogenesis—remains poorly understood. This review aims to systematically outline the mechanisms of hypoxia-related signaling and ncRNA function in breast cancer, with a focus on their molecular interactions in disease progression and their potential clinical implications. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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16 pages, 966 KB

Open AccessReview

Eryptosis in Acute Patients: A Hypothesis on Its Potential Clinical Impact and Current Gaps in Evidence

by Grazia Maria Virzì, Anna Clementi, Monica Zanella and Claudio Ronco

Curr. Issues Mol. Biol. 2026, 48(1), 65; https://doi.org/10.3390/cimb48010065 - 6 Jan 2026

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Abstract

Sepsis is a life-threatening condition driven by a dysregulated host response to infection and remains a leading cause of mortality and morbidity worldwide. Among the many mechanisms implicated in its pathophysiology, the contribution of eryptosis—programmed red blood cell (RBC) death—has been suggested but [...] Read more.

Sepsis is a life-threatening condition driven by a dysregulated host response to infection and remains a leading cause of mortality and morbidity worldwide. Among the many mechanisms implicated in its pathophysiology, the contribution of eryptosis—programmed red blood cell (RBC) death—has been suggested but remains insufficiently investigated. In this hypothesis paper, we propose that eryptosis may represent an underrecognized driver of sepsis-induced anemia and a potential contributor to subsequent organ dysfunction. This hypothesis is supported only by fragmented, predominantly preclinical evidence, which is currently too limited to allow firm conclusions. In this context, we critically revisit the sparse data linking sepsis, endotoxemia, and eryptosis, and outline a testable framework for understanding their possible interaction. We emphasize the substantial gaps in current knowledge, including the absence of robust clinical studies, the heterogeneity of existing experimental models, and persistent uncertainty regarding causality versus mere association. We also explore the theoretical implications of modulating eryptosis as a potential therapeutic approach. Our aim is to stimulate scientific discussion and promote targeted research efforts that may help determine whether addressing eryptosis could ultimately contribute to mitigating anemia, reducing organ injury, and improving outcomes in critically ill patients affected by sepsis. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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28 pages, 924 KB

Open AccessReview

Mapping Lysosomal Storage Disorders with Neurological Features by Cellular Pathways: Towards Precision Medicine

by Anna Makridou, Evangelie Sintou, Sofia Chatzianagnosti, Sofia Gargani, Maria Eleni Manthou, Iasonas Dermitzakis and Paschalis Theotokis

Curr. Issues Mol. Biol. 2025, 47(12), 1009; https://doi.org/10.3390/cimb47121009 - 1 Dec 2025

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Abstract

Lysosomal storage disorders (LSDs) represent a diverse group of inherited metabolic diseases in which impaired lysosomal function leads to progressive accumulation of undegraded substrates and widespread cellular dysfunction. Although traditionally classified according to the type of stored macromolecule, this substrate-based approach often fails [...] Read more.

Lysosomal storage disorders (LSDs) represent a diverse group of inherited metabolic diseases in which impaired lysosomal function leads to progressive accumulation of undegraded substrates and widespread cellular dysfunction. Although traditionally classified according to the type of stored macromolecule, this substrate-based approach often fails to reflect the underlying molecular mechanisms. Recent advances in genetics and cell biology have prompted a shift toward functional classifications that group disorders by the lysosomal pathway disrupted—namely, enzymatic hydrolytic defects, transporter-related defects, biogenesis and signaling defects, and cross-organelle interaction abnormalities. This framework better captures disease complexity and provides a translational roadmap for precision medicine. The neurological system, with its high metabolic demands and vulnerability to impaired clearance mechanisms, is particularly affected, leading to clinical phenotypes ranging from developmental delay to severe neurodegeneration. Genomic technologies and multi-omics platforms have facilitated earlier diagnoses, revealed atypical variants, and informed the development of tailored therapies such as enzyme replacement, substrate reduction, chaperone-based approaches, and gene therapy. The current review proposes a cellular-pathway-oriented framework for classifying LSDs with neurological features and underscores how such an approach can assist in the development of personalized therapeutic strategies. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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29 pages, 796 KB

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Environmental Stressors and Neuroinflammation: Linking Climate Change to Alzheimer’s Disease

by Mario Caldarelli, Pierluigi Rio, Antonio Gasbarrini, Giovanni Gambassi and Rossella Cianci

Curr. Issues Mol. Biol. 2025, 47(11), 959; https://doi.org/10.3390/cimb47110959 - 18 Nov 2025

Cited by 2 | Viewed by 1221

Abstract

Environmental exposures are widely recognized as major risk factors for human health. According to projections by the World Health Organization, climate change is expected to cause a significant increase in mortality within the next few decades. Environmental factors, including diet, weather, occupational exposures, [...] Read more.

Environmental exposures are widely recognized as major risk factors for human health. According to projections by the World Health Organization, climate change is expected to cause a significant increase in mortality within the next few decades. Environmental factors, including diet, weather, occupational exposures, and pollutants play a key role in human diseases affecting different systems, such as cardiovascular, pulmonary, gastrointestinal, and neurological. This narrative review explores the relationship between environmental stressors and neuropathological mechanisms, such as microglial and astrocytic activation, oxidative stress, and neuronal injury, involved in neuroinflammation and the associated neurodegeneration. The pathogenesis and progression of Alzheimer’s disease is discussed in detail, establishing a link between environmental stressors and neuroinflammation. A deeper understanding of these neuropathological mechanisms may guide the development of preventive and therapeutic strategies to safeguard brain health in the context of global environmental change. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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15 pages, 1235 KB

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Competition for Chaperones: A Trade-Off Between Thermotolerance and Antiviral Immunity in Plants

by Almas Madirov, Nurgul Iksat, Zhibek Turarbekova, Bakhytbek Abzhalelov and Zhaksylyk Masalimov

Curr. Issues Mol. Biol. 2025, 47(11), 957; https://doi.org/10.3390/cimb47110957 - 18 Nov 2025

Cited by 1 | Viewed by 799

Abstract

Molecular chaperones HSP70 and HSP90 represent a critical, yet conflict-ridden, node in plant physiology, particularly under the dual impact of heat stress and viral infection. As key components of both thermotolerance (maintaining proteostasis) and innate immunity (stabilization of NLR receptors), they are simultaneously [...] Read more.

Molecular chaperones HSP70 and HSP90 represent a critical, yet conflict-ridden, node in plant physiology, particularly under the dual impact of heat stress and viral infection. As key components of both thermotolerance (maintaining proteostasis) and innate immunity (stabilization of NLR receptors), they are simultaneously exploited by viruses to facilitate their own life cycle. This review critically analyzes this “trilemma,” focusing on the hypothesis of competition for a limited chaperone pool. We present mechanistic insights indicating that during heat stress, cellular priority shifts towards maintaining global proteostasis, thereby diverting chaperones from immune functions. This resource-based competition mechanism potentially explains the collapse of ETI-immunity, as NLR receptors, deprived of support from the HSP90-SGT1-RAR1 complex, are destabilized and targeted for degradation. We also integrate adjacent signaling pathways into this model, including hormonal cross-talk (SA, JA) and autophagy. Understanding this trade-off opens new perspectives for molecular breeding and the biotechnological engineering of stress-resilient crop varieties. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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31 pages, 2984 KB

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Recent Advances in Biosynthesis and Bioactivity of Plant Caffeoylquinic Acids

by Hanqin Chen, Bo Pan, Shilong Zhang, Xin Li, Yuyao Zhang, Kang Gao, Dongliang Chen, Lili Wang, Tianhua Jiang, Chang Luo and Conglin Huang

Curr. Issues Mol. Biol. 2025, 47(11), 942; https://doi.org/10.3390/cimb47110942 - 13 Nov 2025

Cited by 3 | Viewed by 2022

Abstract

Caffeoylquinic acids (CQAs), a class of phenolic acid metabolites widely distributed in plants, encompass 15 positional isomers from mono- to tetra-esters, with 5-O-caffeoylquinic acid (5-CQA) as the predominant form. The biosynthesis of 5-CQA from phenylalanine proceeds through five primary pathways, which are finely [...] Read more.

Caffeoylquinic acids (CQAs), a class of phenolic acid metabolites widely distributed in plants, encompass 15 positional isomers from mono- to tetra-esters, with 5-O-caffeoylquinic acid (5-CQA) as the predominant form. The biosynthesis of 5-CQA from phenylalanine proceeds through five primary pathways, which are finely regulated by environmental, hormonal, and transcription factors from families such as MYB, WRKY, and bHLH. These regulators control 5-CQA synthesis by binding specifically to the promoter regions of key structural genes, including PAL, 4CL and HCT/HQT. Subsequently, 5-CQA serves as a central precursor for the biosynthesis of other CQAs. In terms of bioactivity, CQAs possess remarkable pharmacological activities, encompassing antioxidant, antimicrobial, anti-diabetic, anti-inflammatory and anti-tumor properties. For instance, anti-inflammatory effects are demonstrated by the ability of 5-CQA to reduce key pro-inflammatory cytokines (e.g., TNF-α and IL-1β) and downregulate the TLR4/NF-κB pathway. The synergistic action of 5-CQA with ultraviolet-A reduced succinate-coenzyme Q reductase activity by approximately 72%, highlighting its potential to disrupt bacterial metabolism and combat antibiotic resistance. Furthermore, 3,4,5-triCQA exhibits potent anti-influenza virus activity, potentially through a mechanism distinct from existing neuraminidase inhibitors. Beyond medicine, CQAs show promise in light industry. They serve as antibiotic alternatives in livestock feed to enhance gut health, extend food shelf life through their antioxidant activity, and function as active ingredients in UV-protective skincare formulations. CQAs also enhance plant stress tolerance to cold, arsenic, and pests by mechanisms such as scavenging reactive oxygen species and inhibiting pest mobility. While this review consolidates progress in the biosynthesis and bioactivity of CQAs specifically with caffeoyl substituents, future efforts should leverage modern biotechnological tools and interdisciplinary approaches to bridge critical knowledge gaps in their biosynthesis, transport, and clinical translation. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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21 pages, 1510 KB

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Non-Coding RNAs and Their Role in Maintaining Epidermal Homeostasis

by Daniil D. Romashin, Tatiana V. Tolstova, Alexander L. Rusanov and Natalia G. Luzgina

Curr. Issues Mol. Biol. 2025, 47(11), 924; https://doi.org/10.3390/cimb47110924 - 6 Nov 2025

Cited by 2 | Viewed by 985

Abstract

In recent decades, there has been a significant amount of research on the biological role of non-coding RNAs (ncRNAs) in both normal and pathological conditions. Specifically, a growing body of evidence suggests that ncRNAs play a crucial role in maintaining epidermal homeostasis. These [...] Read more.

In recent decades, there has been a significant amount of research on the biological role of non-coding RNAs (ncRNAs) in both normal and pathological conditions. Specifically, a growing body of evidence suggests that ncRNAs play a crucial role in maintaining epidermal homeostasis. These ncRNAs are involved in regulating epidermal differentiation and wound healing, as well as in pathological skin conditions, such as psoriasis and chronic wounds. The discovery of mechanisms such as RNA interference and other modes of action of ncRNAs has led to the development of novel therapeutic strategies, where ncRNAs could serve as targets, therapeutic agents, or diagnostic markers. This review explores the role of different classes of ncRNAs in the epidermis under normal and abnormal conditions, the mechanisms by which ncRNAs interact with other modulators of epidermal homeostasis, and the current state of ncRNA-based therapy. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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26 pages, 1268 KB

Open AccessReview

Epigenetic Mechanisms in Fabry Disease: A Thematic Analysis Linking Differential Methylation Profiles and Genetic Modifiers to Disease Phenotype

by Jatinder Singh, Paramala Santosh and Uma Ramaswami

Curr. Issues Mol. Biol. 2025, 47(10), 855; https://doi.org/10.3390/cimb47100855 - 16 Oct 2025

Cited by 2 | Viewed by 1063

Abstract

Background/Objectives: Fabry disease is an X-linked lysosomal storage disorder. It is characterised by impaired metabolism of glycosphingolipids whose accumulation causes irreversible organ damage and life-threatening complications. Genotype–phenotype correlations have a limited scope in Fabry disease as the disorder presents with wide-ranging [...] Read more.

Background/Objectives: Fabry disease is an X-linked lysosomal storage disorder. It is characterised by impaired metabolism of glycosphingolipids whose accumulation causes irreversible organ damage and life-threatening complications. Genotype–phenotype correlations have a limited scope in Fabry disease as the disorder presents with wide-ranging clinical variability. In other X-linked disorders, epigenetic profiling has identified methylation patterns and disease modifiers that may explain clinical heterogeneity. In this narrative review and thematic analysis, the role of DNA methylation and epigenetics on the clinical phenotype in Fabry disease was investigated. Methods: Embase, PubMed, and PsycINFO were searched to identify literature on DNA methylation and epigenetics in Fabry disease. Based on the eligibility criteria, 20 articles were identified, and a thematic analysis was performed on the extracted data to identify themes. Results: Three themes emerged: (I) genetic modifiers, (II) methylation profiling, and (III) insights into X chromosome inactivation (XCI). The evidence synthesis revealed that telomere length, especially in early disease stages, bidirectional promoter (BDP) methylation by sphingolipids, epigenetic reader proteins, mitochondrial DNA haplogroups, and DNA methylation of the promoter region of the calcitonin receptor gene are potential genetic modifiers in Fabry disease. Methylation patterns also reveal episignatures in Fabry disease evolution and genes implicated in the maintenance of basement membranes. Studies on XCI further emphasise disease heterogeneity and draw attention to methodological issues in the assessment of XCI. Conclusions: This thematic review shows that DNA methylation and genetic modifiers are key factors modifying clinical variability in Fabry disease. More broadly, it underscores a crucial role for epigenetic processes in driving disease onset, progression, and severity in X-linked disorders. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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15 pages, 1939 KB

Open AccessReview

Challenges of Ozone Therapy in Periodontal Regeneration: A Narrative Review and Possible Therapeutic Improvements

by Nada Tawfig Hashim, Rasha Babiker, Vivek Padmanabhan, Md Sofiqul Islam, Sivan Padma Priya, Nallan C. S. K. Chaitanya, Riham Mohammed, Shahistha Parveen Dasnadi, Ayman Ahmed, Bakri Gobara Gismalla and Muhammed Mustahsen Rahman

Curr. Issues Mol. Biol. 2025, 47(10), 811; https://doi.org/10.3390/cimb47100811 - 1 Oct 2025

Cited by 2 | Viewed by 2216

Abstract

Ozone (O₃) has re-emerged in periodontology for its antimicrobial, oxygenating, and immunomodulatory actions, yet its role in regeneration remains contentious. This narrative review synthesizes current evidence on adjunctive ozone use in periodontal therapy, delineates cellular constraints—especially in periodontal ligament fibroblasts (PDLFs)—and [...] Read more.

Ozone (O₃) has re-emerged in periodontology for its antimicrobial, oxygenating, and immunomodulatory actions, yet its role in regeneration remains contentious. This narrative review synthesizes current evidence on adjunctive ozone use in periodontal therapy, delineates cellular constraints—especially in periodontal ligament fibroblasts (PDLFs)—and explores mitigation strategies using bioactive compounds and advanced delivery platforms. Two recent meta-analyses indicate that adjunctive ozone with scaling and root planing yields statistically significant reductions in probing depth and gingival inflammation, with no significant effects on bleeding on probing, plaque control, or clinical attachment level; interpretation is limited by heterogeneity of formulations, concentrations, and delivery methods. Mechanistically, ozone imposes a dose-dependent oxidative burden that depletes glutathione and inhibits glutathione peroxidase and superoxide dismutase, precipitating lipid peroxidation, mitochondrial dysfunction, ATP depletion, and PDLF apoptosis. Concurrent activation of NF-κB and upregulation of IL-6/TNF-α, together with matrix metalloproteinase-mediated extracellular matrix degradation and tissue dehydration (notably with gaseous applications), further impairs fibroblast migration, adhesion, and ECM remodeling, constraining regenerative potential. Emerging countermeasures include co-administration of polyphenols (epigallocatechin-3-gallate, resveratrol, curcumin, quercetin), coenzyme Q10, vitamin C, and hyaluronic acid to restore redox balance, stabilize mitochondria, down-modulate inflammatory cascades, and preserve ECM integrity. Nanocarrier-based platforms (nanoemulsions, polymeric nanoparticles, liposomes, hydrogels, bioadhesive films) offer controlled ozone release and co-delivery of protectants, potentially widening the therapeutic window while minimizing cytotoxicity. Overall, current evidence supports ozone as an experimental adjunct rather than a routine regenerative modality. Priority research needs include protocol standardization, dose–response definition, long-term safety, and rigorously powered randomized trials evaluating bioactive-ozone combinations and nanocarrier systems in clinically relevant periodontal endpoints. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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20 pages, 1341 KB

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Mechanisms of Silique Dehiscence in Rapeseed: A Review of Research Progress

by Menglin Zhou, Wuming Deng, Bingbing Dai, Qingqing Yu, Wei Zhou, Xiaofei Zan and Xi Song

Curr. Issues Mol. Biol. 2025, 47(9), 755; https://doi.org/10.3390/cimb47090755 - 12 Sep 2025

Cited by 1 | Viewed by 1128

Abstract

Silique dehiscence is a critical biological phenomenon in rapeseed production that significantly influences seed maturity, harvesting efficiency, and ultimately yield. As one of the world’s most important oilseed crops, studying the mechanisms underlying silique dehiscence in rapeseed (Brassica napus L.) not only [...] Read more.

Silique dehiscence is a critical biological phenomenon in rapeseed production that significantly influences seed maturity, harvesting efficiency, and ultimately yield. As one of the world’s most important oilseed crops, studying the mechanisms underlying silique dehiscence in rapeseed (Brassica napus L.) not only aids in understanding fundamental principles of plant development but also provides a scientific basis for optimizing agricultural production practices. Silique dehiscence occurs naturally during the maturation process of rapeseed, with the timing and extent of this phenomenon directly affecting seed harvesting efficiency. This paper reviews the research progress regarding the mechanization of canola production, which enhances harvesting efficiency by enabling timely harvest coordination to minimize pre-harvest shattering losses and reduce post-harvest seed damage. Additionally, it addresses the factors influencing pod shattering, the process of pod shattering, the genes associated with this phenomenon, and the molecular mechanisms underlying pod shattering. These findings establish a foundation for a comprehensive understanding of pod shattering in canola. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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16 pages, 931 KB

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Myo-Inositol Oxygenase (MIOX): A Pivotal Regulator and Therapeutic Target in Multiple Diseases

by Shaocong Han, Min Zhang, Huan Yang, Huiqiong Yang, Yanmei Tang, Weixi Li, Li Li, Jie Yu and Xingxin Yang

Curr. Issues Mol. Biol. 2025, 47(9), 745; https://doi.org/10.3390/cimb47090745 - 11 Sep 2025

Cited by 1 | Viewed by 1821

Abstract

Myo-inositol oxygenase (MIOX), as the sole enzyme catalyzing myo-inositol (MI) catabolism in mammals, plays a central role in maintaining intracellular MI homeostasis. Dysregulation of MIOX activity disrupts MI metabolic balance, leading to pathological processes including oxidative stress, inflammation, and ferroptosis, which subsequently induce [...] Read more.

Myo-inositol oxygenase (MIOX), as the sole enzyme catalyzing myo-inositol (MI) catabolism in mammals, plays a central role in maintaining intracellular MI homeostasis. Dysregulation of MIOX activity disrupts MI metabolic balance, leading to pathological processes including oxidative stress, inflammation, and ferroptosis, which subsequently induce multiple diseases such as metabolic syndrome, neurological disorders, tumors, and reproductive/developmental disorders. This article systematically reviews the structure and function of MIOX as well as the pathological consequences arising from its dysregulation. Although its pathological significance is increasingly recognized, the molecular mechanisms of MIOX in many diseases have not been fully elucidated, and targeted modulators of MIOX are lacking. Future research should focus on the in-depth elucidation of the pathogenic mechanisms of MIOX disorders and the development of MIOX modulators, thereby providing precise therapeutic strategies for related diseases. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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43 pages, 4194 KB

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Metabolic Engineering of Terpenoid Biosynthesis in Medicinal Plants: From Genomic Insights to Biotechnological Applications

by Changfeng Guo, Si Xu and Xiaoyun Guo

Curr. Issues Mol. Biol. 2025, 47(9), 723; https://doi.org/10.3390/cimb47090723 - 5 Sep 2025

Cited by 6 | Viewed by 5246

Abstract

Terpenoids, which are essential pharmaceutical compounds, encounter significant production challenges due to their low yields in native plants and associated ecological concerns. This review summarizes recent advances in metabolic engineering strategies applied across three complementary platforms: native medicinal plants, microbial systems, and heterologous [...] Read more.

Terpenoids, which are essential pharmaceutical compounds, encounter significant production challenges due to their low yields in native plants and associated ecological concerns. This review summarizes recent advances in metabolic engineering strategies applied across three complementary platforms: native medicinal plants, microbial systems, and heterologous plant hosts. We present how the “Genomic Insights to Biotechnological Applications” paradigm, supported by multi-omics technologies such as genomics, transcriptomics, metabolomics, and related disciplines, contributes to advancing research in this field. These technologies enable the systematic identification of key biosynthetic genes and regulatory networks. CRISPR-based tools, enzyme engineering, and subcellular targeting are presented as pivotal transformative strategies in advancing metabolic engineering approaches. Strategic co-expression and optimization approaches have achieved substantial improvements in product yields, as demonstrated by a 25-fold increase in paclitaxel production and a 38% enhancement in artemisinin yield. Persistent challenges, such as metabolic flux balancing, cytotoxicity, and scale-up economics, are discussed in conjunction with emerging solutions, including machine learning and photoautotrophic chassis systems. We conclude by proposing a strategic roadmap for industrial translation that highlights the essential integration of systems biology and synthetic biology approaches to accelerate the transition of terpenoid biomanufacturing from discovery to commercial-scale application. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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19 pages, 733 KB

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Methane, Bacteria, Fungi, and Fermentation: Pathophysiology, Diagnosis and Treatment Strategies for Small Intestinal Bacterial Overgrowth, Intestinal Methanogen Overgrowth and Small Intestinal Fungal Overgrowth

by Adam Wawrzeńczyk, Marta Czarnowska, Samira Darwish, Aleksandra Ćwirko-Godycka, Kinga Lis, Maciej Szota, Paweł Treichel, Aleksandra Wojtkiewicz and Katarzyna Napiórkowska-Baran

Curr. Issues Mol. Biol. 2025, 47(9), 713; https://doi.org/10.3390/cimb47090713 - 2 Sep 2025

Cited by 2 | Viewed by 8960

Abstract

The human gastrointestinal tract hosts a complex ecosystem known as the gut microbiota, which plays a crucial part in digestion and immune system function. Among the clinically recognized manifestations of dysbiosis in this system are Small Intestinal Bacterial Overgrowth (SIBO), Intestinal Methanogen Overgrowth [...] Read more.

The human gastrointestinal tract hosts a complex ecosystem known as the gut microbiota, which plays a crucial part in digestion and immune system function. Among the clinically recognized manifestations of dysbiosis in this system are Small Intestinal Bacterial Overgrowth (SIBO), Intestinal Methanogen Overgrowth (IMO), Small Intestinal Fungal Overgrowth (SIFO), and Large Intestinal Bacterial Overgrowth (LIBO). This study aims to investigate the complex pathophysiological mechanisms underlying these syndromes and their diagnostics and therapeutic options, focusing primarily on the roles of methane-producing archaea and fungal overgrowth. The methods employed in this study involve a comprehensive analysis and synthesis of peer-reviewed articles, systematic reviews, clinical trials, and meta-analyses. This review summarizes that methane production by Methanobrevibacter smithii was linked to altered fermentation, reduced microbial diversity, and slowed intestinal transit. Fungal species were associated with increased intestinal permeability, inflammation, and biofilm formation. Targeted interventions addressing microbial imbalances demonstrated potential therapeutic value. This review highlights the complex and multifactorial nature of gut dysbiosis, revealing its impact beyond the gastrointestinal tract. While emerging therapies targeting methanogens, fungi, and biofilms show promise, further research is essential to optimize their clinical application. The findings emphasize the need for interdisciplinary collaboration to refine diagnostic and therapeutic strategies. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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17 pages, 2011 KB

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A Narrative Review of Heavy Metals and Sperm Quality: The Interplay with Antioxidant Imbalance and Reactive Oxygen Species

by Soukaina Azil, Khaoula Errafii, Moncef Benkhalifa, Noureddine Louanjli, Bouchra Ghazi and Salsabil Hamdi

Curr. Issues Mol. Biol. 2025, 47(8), 650; https://doi.org/10.3390/cimb47080650 - 13 Aug 2025

Cited by 6 | Viewed by 3969

Abstract

Reproductive infertility is characterized by the inability to achieve pregnancy after a year or more of unprotected sexual intercourse. This review highlights the significant impact of exposure to both types of heavy metals (essential and non-essential) on the reproductive performance of various species, [...] Read more.

Reproductive infertility is characterized by the inability to achieve pregnancy after a year or more of unprotected sexual intercourse. This review highlights the significant impact of exposure to both types of heavy metals (essential and non-essential) on the reproductive performance of various species, particularly humans. Heavy metals present a high atomic density and weight, including lead, mercury, cadmium, nickel, chromium, and arsenic, and are delivered into the environment through natural and human activities, posing a threat to ecological systems and human reproductive health. These heavy metals have the potential for bioaccumulation and can adversely affect male fertility and sperm quality due to their role in disrupting endocrine functions, altering hormone levels responsible for sperm production, and inducing oxidative stress. The elevated production of reactive oxygen species (ROS) exceeds the capability of antioxidants and can lead to the alteration of sperm quality. Seminal fluid contains antioxidants like vitamin C, vitamin E, zinc, and selenium to counteract the impacts of ROS and also to preserve the sperm function. This review aims also to explore the impact of heavy metals on sperm quality and their relationship with antioxidant imbalance and ROS. The exposure to heavy metals whether through occupational or environmental means increases the production of ROS and therefore leads to an imbalance of antioxidants production. All these factors have no doubt an impact on male reproductive health. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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14 pages, 4774 KB

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Biochemical Battle: Influence of Omega-6 Fatty Acids on the Formation of DNA Adducts with 4-HNE

by Edyta Błaszczyk and Bolesław T. Karwowski

Curr. Issues Mol. Biol. 2025, 47(8), 645; https://doi.org/10.3390/cimb47080645 - 12 Aug 2025

Viewed by 3782

Abstract

While omega-6 fatty acids play an important role in normal cell function, their excess in the diet is associated with an increased risk of developing diseases such as obesity, non-alcoholic fatty liver disease (NAFLD), inflammatory bowel disease (IBD) and Alzheimer’s disease. Furthermore, excessive [...] Read more.

While omega-6 fatty acids play an important role in normal cell function, their excess in the diet is associated with an increased risk of developing diseases such as obesity, non-alcoholic fatty liver disease (NAFLD), inflammatory bowel disease (IBD) and Alzheimer’s disease. Furthermore, excessive intake has been shown to lead to chronic inflammation, which is related to increased production of reactive oxygen species (ROS). This conditioncan initiate lipid peroxidation in cell membranes, leading to the degradation of their fatty acids. One of the main products of omega-6 peroxidation is the α,β-unsaturated aldehyde, i.e., 4-hydroxynonenal (4-HNE), which is able to form four diastereoisomeric adducts with guanine. These 4-HNE adducts have been identified in the DNA of humans and rodents. Depending on their stereochemistry, they are able to influence double helix stability and cause DNA–DNA or DNA–Protein cross-links. Moreover, studies have shown that 4-HNE adducts formed in the human genome are considered mutation hotspots in hepatocellular carcinoma. Although the cell possesses defence mechanisms, without a well-balanced diet allowing correct cell function, they may not be sufficient to protect the genetic code. This review provides an overview of the molecular mechanisms underlying oxidative stress, lipid peroxidation, and the formation of DNA adducts. Particular emphasis is placed on the role of an omega-6-rich diet in inflammatory diseases, and on the formation of 4-HNE, which is a major product of lipid peroxidation, and its broader implications for genome stability, ageing, and disease progression. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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14 pages, 594 KB

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The Aging Lung: Exploring Multimorbidity Patterns and Their Clinical Implications: A Narrative Review

by Ali Albarrati and Nichola S. Gale

Curr. Issues Mol. Biol. 2025, 47(7), 561; https://doi.org/10.3390/cimb47070561 - 18 Jul 2025

Cited by 1 | Viewed by 2211

Abstract

Aging is a multifaceted biological process characterized by a progressive decline in cellular function and physiological resilience, increasing the risk of multiple chronic conditions. Chronic lung diseases frequently manifest within the aging population and are closely intertwined with systemic dysfunctions across cardiovascular, musculoskeletal, [...] Read more.

Aging is a multifaceted biological process characterized by a progressive decline in cellular function and physiological resilience, increasing the risk of multiple chronic conditions. Chronic lung diseases frequently manifest within the aging population and are closely intertwined with systemic dysfunctions across cardiovascular, musculoskeletal, and neurological systems. In this review, we explore the biological mechanisms linking aging, multiple chronic conditions patterns, and chronic lung disease, with a particular focus on inflammaging and cellular aging. We also highlight shared pathological pathways such as oxidative stress, mitochondrial dysfunction, and the dysregulation of repair processes that underlie both natural aging and the accelerated aging seen in chronic lung disease. Additionally, we discuss the systemic impact of multiple chronic conditions on patient outcomes, including increased frailty, diminished physical capacity, cognitive impairment, and elevated mortality risk. This review advocates for a comprehensive, patient-centered approach that combines early detection, personalized pharmacological therapies targeting inflammatory and senescent pathways, and non-pharmacological interventions such as pulmonary rehabilitation, exercise, and dietary optimization. Emerging therapeutics, including senolytics and anti-inflammatory agents, present promising avenues for mitigating age-related lung decline and managing multiple chronic conditions. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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29 pages, 538 KB

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Dynamic Rendition of Adipose Genes Under Epigenetic Regulation: Revealing New Mechanisms of Obesity Occurrence

by Weijing Wen, Simeng Gu, Fanjia Guo, Zhijian Chen, Sujun Yan and Zhe Mo

Curr. Issues Mol. Biol. 2025, 47(7), 540; https://doi.org/10.3390/cimb47070540 - 11 Jul 2025

Viewed by 3730

Abstract

Obesity is a chronic metabolic disorder and a growing global public health challenge, affecting hundreds of millions of individuals worldwide. While diet and physical activity are well-established contributors, increasing evidence underscores the critical role of epigenetic mechanisms in mediating obesity-related processes. Epigenetic modifications—such [...] Read more.

Obesity is a chronic metabolic disorder and a growing global public health challenge, affecting hundreds of millions of individuals worldwide. While diet and physical activity are well-established contributors, increasing evidence underscores the critical role of epigenetic mechanisms in mediating obesity-related processes. Epigenetic modifications—such as DNA methylation, RNA methylation (particularly N6-methyladenosine), histone modifications, non-coding RNAs, and chromatin remodeling—modulate gene expression without altering the DNA sequence. This review aims to provide an overview of the epigenetic mechanisms involved in obesity, with an emphasis on their molecular functions and regulatory networks. Integrating findings from relevant studies, we discuss how these modifications influence obesity-related outcomes through regulating key processes such as adipocyte differentiation and energy metabolism. Advancing our understanding of epigenetic regulation may pave the way for novel, targeted strategies in the prevention and treatment of obesity. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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20 pages, 581 KB

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Mapping Disorders with Neurological Features Through Mitochondrial Impairment Pathways: Insights from Genetic Evidence

by Anna Makridou, Evangelie Sintou, Sofia Chatzianagnosti, Iasonas Dermitzakis, Sofia Gargani, Maria Eleni Manthou and Paschalis Theotokis

Curr. Issues Mol. Biol. 2025, 47(7), 504; https://doi.org/10.3390/cimb47070504 - 1 Jul 2025

Cited by 1 | Viewed by 2223

Abstract

Mitochondrial dysfunction is a key driver of neurological disorders due to the brain’s high energy demands and reliance on mitochondrial homeostasis. Despite advances in genetic characterization, the heterogeneity of mitochondrial diseases complicates diagnosis and treatment. Mitochondrial dysfunction spans a broad clinical spectrum, from [...] Read more.

Mitochondrial dysfunction is a key driver of neurological disorders due to the brain’s high energy demands and reliance on mitochondrial homeostasis. Despite advances in genetic characterization, the heterogeneity of mitochondrial diseases complicates diagnosis and treatment. Mitochondrial dysfunction spans a broad clinical spectrum, from early-onset encephalopathies to adult neurodegeneration, with phenotypic and genetic variability necessitating integrated models of mitochondrial neuropathology. Mutations in nuclear or mitochondrial DNA disrupt energy production, induce oxidative stress, impair mitophagy and biogenesis, and lead to neuronal degeneration and apoptosis. This narrative review provides a structured synthesis of current knowledge by classifying mitochondrial-related neurological disorders according to disrupted biochemical pathways, in order to clarify links between genetic mutations, metabolic impairments, and clinical phenotypes. More specifically, a pathway-oriented framework was adopted that organizes disorders based on the primary mitochondrial processes affected: oxidative phosphorylation (OXPHOS), pyruvate metabolism, fatty acid β-oxidation, amino acid metabolism, phospholipid remodeling, multi-system interactions, and neurodegeneration with brain iron accumulation. Genetic, clinical and molecular data were analyzed to elucidate shared and distinct pathophysiological features. A comprehensive table synthesizes genetic causes, inheritance patterns, and neurological manifestations across disorders. This approach offers a conceptual framework that connects molecular findings to clinical practice, supporting more precise diagnostic strategies and the development of targeted therapies. Advances in whole-exome sequencing, pharmacogenomic profiling, mitochondrial gene editing, metabolic reprogramming, and replacement therapy—promise individualized therapeutic approaches, although hurdles including heteroplasmy, tissue specificity, and delivery challenges must be overcome. Ongoing molecular research is essential for translating these advances into improved patient care and quality of life. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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38 pages, 916 KB

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The Impact and Molecular Mechanisms of Exercise in Cancer Therapy

by Yingjie Sun, Yixiao Ma, Lei Shi, Tong Liu, Yahong Dong and Qiguan Jin

Curr. Issues Mol. Biol. 2025, 47(5), 374; https://doi.org/10.3390/cimb47050374 - 20 May 2025

Cited by 7 | Viewed by 8641

Abstract

Cancer is a major global health issue, and exercise has become a key supportive treatment. It contributes to reducing cancer risk, enhancing prognosis, and aiding recovery, especially for survivors. However, the exact mechanisms, such as how exercise reduces cancer risk or enhances treatment, [...] Read more.

Cancer is a major global health issue, and exercise has become a key supportive treatment. It contributes to reducing cancer risk, enhancing prognosis, and aiding recovery, especially for survivors. However, the exact mechanisms, such as how exercise reduces cancer risk or enhances treatment, are still unclear. Current research often focuses on specific cancer types, ignoring the diverse needs of patients. This limits the development of personalized exercise plans. Additionally, there is insufficient comparison of exercise types—like aerobic, resistance, and high-intensity interval training—regarding their adverse effects and long-term benefits. The best combination of exercises and personalized strategies remains unknown. This review underscores the contribution of physical exercise to cancer prevention and treatment, emphasizing its positive effects on reducing fatigue, improving physical strength, and enhancing mental health. It also explores the molecular mechanisms of regulating tumor immunity and energy metabolism. Additionally, the article covers criteria for selecting exercise types and intensities, and the development of personalized exercise plans. Finally, it provides guidelines for exercise prescriptions and suggests future research directions to improve interventions for cancer patients. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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16 pages, 1396 KB

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Therapeutic Potential of Alpha-Lipoic Acid: Unraveling Its Role in Oxidative Stress and Inflammatory Conditions

by Aqsa Shahid, Khadeeja Nasir and Madhav Bhatia

Curr. Issues Mol. Biol. 2025, 47(5), 322; https://doi.org/10.3390/cimb47050322 - 30 Apr 2025

Cited by 15 | Viewed by 16285

Abstract

Alpha-lipoic acid (ALA) is an essential organosulfur compound with a wide range of therapeutic applications, particularly in conditions involving inflammation and oxidative stress. In this review, we describe our current understanding of the multifaceted role of ALA in several inflammatory diseases (acute pancreatitis, [...] Read more.

Alpha-lipoic acid (ALA) is an essential organosulfur compound with a wide range of therapeutic applications, particularly in conditions involving inflammation and oxidative stress. In this review, we describe our current understanding of the multifaceted role of ALA in several inflammatory diseases (acute pancreatitis, arthritis, osteoarthritis, asthma, and sepsis), cardiovascular disorders (CVDs), and neurological conditions. The dual redox nature of ALA, shared with its reduced form dihydrolipoic acid (DHLA), underpins its powerful antioxidant and anti-inflammatory properties, including reactive oxygen species scavenging, metal chelation, and the regeneration of endogenous antioxidants such as glutathione. A substantial body of evidence from preclinical and clinical studies suggests that ALA modulates the key signaling pathways involved in inflammation and cellular stress responses, making it a promising candidate for mitigating inflammation and its systemic consequences. Notably, we also discuss a novel perspective that attributes some of the therapeutic effects of ALA to its ability to release hydrogen sulfide (H₂S), a gaseous signaling molecule. This mechanism may offer further insights into the efficacy of ALA in the treatment of several diseases. Together, these findings support the potential of ALA as a multifunctional agent for managing inflammatory and oxidative stress-related diseases. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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18 pages, 3588 KB

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FNIP1 Deficiency: Pathophysiology and Clinical Manifestations of a Rare Syndromic Primary Immunodeficiency

by Samuele Roncareggi, Brian M. Iritani and Francesco Saettini

Curr. Issues Mol. Biol. 2025, 47(4), 290; https://doi.org/10.3390/cimb47040290 - 18 Apr 2025

Viewed by 1790

Abstract

Folliculin-interacting protein 1 (FNIP1) is a key regulator of cellular metabolism and immune homeostasis, integrating nutrient signaling with proteostasis. FNIP1 forms a complex with folliculin (FLCN) to regulate the mechanistic target of rapamycin complex 1 (mTORC1), functioning as a GTPase-activating protein (GAP) for [...] Read more.

Folliculin-interacting protein 1 (FNIP1) is a key regulator of cellular metabolism and immune homeostasis, integrating nutrient signaling with proteostasis. FNIP1 forms a complex with folliculin (FLCN) to regulate the mechanistic target of rapamycin complex 1 (mTORC1), functioning as a GTPase-activating protein (GAP) for RagC/D. Additionally, FNIP1 interacts with heat shock protein 90 (HSP90) and undergoes phosphorylation, glycosylation, and ubiquitination, which dynamically regulate its stability and function. Evidence from murine models suggests that FNIP1 loss disrupts immune cell development and mitochondrial homeostasis. However, FNIP1 deficiency in humans remains incompletely characterized, and its full phenotypic spectrum is likely underestimated. Notably, FNIP1-deficient patients exhibit immunological and hematological abnormalities, immune dysregulation, and metabolic perturbations, emphasizing its role in cellular adaptation to stress. Understanding the mechanistic basis of FNIP1 dysfunction in human tissues will be critical for delineating its contributions to immune and metabolic disorders and identifying targeted interventions. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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29 pages, 1210 KB

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Recent Advances in Bone Tissue Engineering: Enhancing the Potential of Mesenchymal Stem Cells for Regenerative Therapies

by Milena Kostadinova, Miryana Raykovska, Radoil Simeonov, Stephan Lolov and Milena Mourdjeva

Curr. Issues Mol. Biol. 2025, 47(4), 287; https://doi.org/10.3390/cimb47040287 - 17 Apr 2025

Cited by 16 | Viewed by 7411

Abstract

Bone tissue engineering (BTE) has emerged as a promising strategy for addressing bone defects and disorders that cannot be repaired through traditional methods. This field leverages the potential of various biomaterials, cells, and bioactive factors to promote bone regeneration. Mesenchymal stem cells (MSCs) [...] Read more.

Bone tissue engineering (BTE) has emerged as a promising strategy for addressing bone defects and disorders that cannot be repaired through traditional methods. This field leverages the potential of various biomaterials, cells, and bioactive factors to promote bone regeneration. Mesenchymal stem cells (MSCs) have gained significant attention due to their osteogenic potential, which can be enhanced through osteoinductive factors. Osteoinductive factors, including growth factors like BMPs, TGF-β, VEGF, and IGF, play a crucial role in stimulating the osteodifferentiation process, thereby promoting bone regeneration. Furthermore, bioprinting technologies have opened new avenues for precisely designing scaffolds that can mimic the native bone architecture and provide a conducive environment for MSC differentiation. The integration of bioprinting with mesenchymal stem cells and osteoinductive factors has the potential to revolutionize regenerative therapies by allowing for the creation of patient-specific bone grafts. This review highlights the latest developments in MSC-based therapies, the role of osteoinductive factors, and the impact of bioprinting in advancing BTE. It also discusses future directions for improving the efficacy and clinical translation of these technologies. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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13 pages, 561 KB

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T Cell Repertoire Analysis as a Molecular Signature of the Spectrum of T-LGL Lymphoproliferative Disorders: Tracing the Literature

by Evangelia Stalika and Ioannis Tsamesidis

Curr. Issues Mol. Biol. 2025, 47(4), 264; https://doi.org/10.3390/cimb47040264 - 8 Apr 2025

Viewed by 1198

Abstract

CD3⁺ CD8⁺ CD57⁺ mono-, oligo-, and poly-clonal expansions, both idiopathic and clinically related diseases, including as autoimmunity, viral infections, post-transplant, and hematologic malignancies, can cause T large granular lymphocyte (T-LGL) lymphoproliferative disorders. It is yet unknown if this variability is [...] Read more.

CD3⁺ CD8⁺ CD57⁺ mono-, oligo-, and poly-clonal expansions, both idiopathic and clinically related diseases, including as autoimmunity, viral infections, post-transplant, and hematologic malignancies, can cause T large granular lymphocyte (T-LGL) lymphoproliferative disorders. It is yet unknown if this variability is a result of a dynamic process of cytotoxic T cell responses to exoantigens and autoantigens. The major aim of this review is to gather evidence from the literature in order to further highlight the possible pathogenetic mechanism that may underly the above clinical entities. Major research findings include the following: (i) pronounced skewing of the TRBV repertoire; (ii) existence of more than one immunodominant clonotype; (iii) persistent clonotypes in different timepoints albeit with fluctuating frequencies (clonal drift); and (iv) shared (‘public’) clonotypes between cases and the public databases, further suggesting a limited number of antigens implicated in pathogenesis of T-LGL cases. However, there is no clear distinction between polyclonal, oligoclonal, and monoclonal T-LGL lymphoproliferative conditions; rather, the progression from a polyclonal cytotoxic response to the emergence of T-LGL leukemia is slow. In the ontogeny and evolution of T-LGL leukemia, repertoire limits, public clonotypes, and clonal drift all clearly show selection by limited (perhaps shared) antigens. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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25 pages, 3464 KB

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Different Species of Bats: Genomics, Transcriptome, and Immune Repertoire

by Huifang Wang, Hao Zhou and Xinsheng Yao

Curr. Issues Mol. Biol. 2025, 47(4), 252; https://doi.org/10.3390/cimb47040252 - 7 Apr 2025

Cited by 1 | Viewed by 3671

Abstract

Bats are the only mammals with the ability to fly and are the second largest order after rodents, with 20 families and 1213 species (over 3000 subspecies) and are widely distributed in regions around the world except for Antarctica. What makes bats unique [...] Read more.

Bats are the only mammals with the ability to fly and are the second largest order after rodents, with 20 families and 1213 species (over 3000 subspecies) and are widely distributed in regions around the world except for Antarctica. What makes bats unique are their biological traits: a tolerance to zoonotic infections without getting clinical symptoms, long lifespans, a low incidence of tumors, and a high metabolism. As a result, they are receiving increasing attention in the field of life sciences, particularly in medical research. The rapid advancements in sequencing technology have made it feasible to comprehensively analyze the diverse biological characteristics of bats. This review comprehensively discusses the following: (1) The assembly and annotation overview of 77 assemblies from 54 species across 11 families and the transcriptome sequencing overview of 42 species from 7 families, focused on a comparative analysis of genomic architecture, sensory adaptations (auditory, visual, and olfactory), and immune functions. Key findings encompass marked interspecies divergence in genome size, lineage-specific expansions/contractions of immune-related gene families (APOBEC, IFN, and PYHIN), and sensory gene adaptations linked to ecological niches. Notably, echolocating bats exhibited convergent evolution in auditory genes (SLC26A5 and FOXP2), while fruit-eating bats displayed a degeneration of vision-associated genes (RHO), reflecting trade-offs between sensory specialization and ecological demands. (2) The annotation of the V (variable), D (diversity), J (joining), and C (constant) gene families in the TR and IG loci of 12 species from five families, with a focus on a comparative analysis of the differences in TR and IG genes and CDR3 repertoires between different bats and between bats and other mammals, provides us with a deeper understanding of the development and function of the immune system in organisms. Integrated genomic, transcriptomic, and immune repertoire analyses reveal that bats employ distinct antiviral strategies, primarily mediated by enhanced immune tolerance and suppressed inflammatory responses. This review provides foundational information, collaboration directions, and new perspectives for various laboratories conducting basic and applied research on the vast array of bat biology. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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17 pages, 860 KB

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Signaling Mechanism of Budding, Proliferation, and Tissue Regeneration in Cnidaria

by Jie Lv, Jinhong Chen, Liangzhi Li, Xiaoyu Geng, Bingbing Li, Mingke Wang and Jishun Yang

Curr. Issues Mol. Biol. 2025, 47(4), 219; https://doi.org/10.3390/cimb47040219 - 24 Mar 2025

Cited by 1 | Viewed by 2911

Abstract

Phylum Cnidaria occupies an early branching position in the evolution of eukaryotes, establishing both close and distant relationships with most other eukaryotic metazoans. Budding encompasses the complete processes of cell proliferation, differentiation, and tissue regeneration, making it an ideal model for exploring various [...] Read more.

Phylum Cnidaria occupies an early branching position in the evolution of eukaryotes, establishing both close and distant relationships with most other eukaryotic metazoans. Budding encompasses the complete processes of cell proliferation, differentiation, and tissue regeneration, making it an ideal model for exploring various aspects of cellular function and evolution. Additionally, budding serves as the primary reproductive method for increasing the cnidarian population. This asexual reproductive phase is critical for managing and mitigating cnidarian outbreaks. This paper summarizes the common factors influencing budding, the signaling pathways involved and their associated functions, and the methodologies employed in relevant research, providing a theoretical foundation for the prevention and control of cnidarian populations. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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18 pages, 583 KB

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Adaptations of the Genus Bradyrhizobium to Selected Elements, Heavy Metals and Pesticides Present in the Soil Environment

by Joanna Banasiewicz, Aleksandra Gumowska, Agata Hołubek and Sławomir Orzechowski

Curr. Issues Mol. Biol. 2025, 47(3), 205; https://doi.org/10.3390/cimb47030205 - 18 Mar 2025

Cited by 6 | Viewed by 2725

Abstract

Rhizobial bacteria perform a number of extremely important functions in the soil environment. In addition to fixing molecular nitrogen and transforming it into a form available to plants, they participate in the circulation of elements and the decomposition of complex compounds present in [...] Read more.

Rhizobial bacteria perform a number of extremely important functions in the soil environment. In addition to fixing molecular nitrogen and transforming it into a form available to plants, they participate in the circulation of elements and the decomposition of complex compounds present in the soil, sometimes toxic to other organisms. This review article describes the molecular mechanisms occurring in the most diverse group of rhizobia, the genus Bradyrhizobium, allowing these bacteria to adapt to selected substances found in the soil. Firstly, the adaptation of bradyrhizobia to low and high concentrations of elements such as iron, phosphorus, sulfur, calcium and manganese was shown. Secondly, the processes activated in their cells in the presence of heavy metals such as lead, mercury and arsenic, as well as radionuclides, were described. Additionally, due to the potential use of Bradyrhziobium as biofertilizers, their response to pesticides commonly used in agriculture, such as glyphosate, sulfentrazone, chlorophenoxy herbicides, flumioxazine, imidazolinone, atrazine, and insecticides and fungicides, was also discussed. The paper shows the great genetic diversity of bradyrhizobia in terms of adapting to variable environmental conditions present in the soil. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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16 pages, 1944 KB

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A Comprehensive Review Exploring the Role of Bone Morphogenetic Proteins [BMP]: Biological Mechanisms

by Akanksha A. Kalal and Satyajit Mohapatra

Curr. Issues Mol. Biol. 2025, 47(3), 156; https://doi.org/10.3390/cimb47030156 - 27 Feb 2025

Cited by 6 | Viewed by 6542

Abstract

Bone morphogenetic proteins (BMPs) belong to the TGF-β family. They perform diverse roles in development, osteogenesis, and vasculogenesis. BMPs have crucial functions in embryonic development and regulate the specialization of various cell types. The dysregulation of BMP activity at various stages in signal [...] Read more.

Bone morphogenetic proteins (BMPs) belong to the TGF-β family. They perform diverse roles in development, osteogenesis, and vasculogenesis. BMPs have crucial functions in embryonic development and regulate the specialization of various cell types. The dysregulation of BMP activity at various stages in signal transduction is associated with a diverse range of human diseases. It is not surprising that BMPs also have a role in tumor formation and control the progression of cancer through different phases. Nevertheless, their specific roles remain ambiguous and the findings regarding this have been inconsistent. The objective of this review is to highlight the important functions of BMP ligands, receptors, and signaling mediators and the subsequent effects on final cellular responses resulting from these signaling modalities. This review elucidates the dysregulation of BMPs identified in various cancer types, which serves as a predictive sign for favorable results in cancer therapy. Alterations in the BMP pathway can represent a crucial milestone in the genetic and molecular mechanisms that facilitate cancer formation. This review has shown that alterations in certain components of the BMP pathway are evident in various tumor forms, including breast, gastric, colorectal, and myeloma cancer. This review reinforces the conclusion that BMPs exert both beneficial and detrimental effects on cancer biology. Collectively, these findings indicate that BMPs serve multiple functions in cancer; therefore, directing therapeutic efforts to focus on BMP may be a highly effective method for treating several cancers. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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12 pages, 831 KB

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Research Progress on the Relationship Between PRPF8 and Cancer

by Guoqing Huang, Dandan Wang and Jiaying Xue

Curr. Issues Mol. Biol. 2025, 47(3), 150; https://doi.org/10.3390/cimb47030150 - 26 Feb 2025

Cited by 1 | Viewed by 2678

Abstract

Alternative splicing (AS) plays a crucial role in regulating gene expression and protein diversity, influencing both normal cellular function and pathological conditions, including cancer. Protein pre-mRNA processing factor 8 (PRPF8), a core component of the spliceosome, is integral to the splicing process, ensuring [...] Read more.

Alternative splicing (AS) plays a crucial role in regulating gene expression and protein diversity, influencing both normal cellular function and pathological conditions, including cancer. Protein pre-mRNA processing factor 8 (PRPF8), a core component of the spliceosome, is integral to the splicing process, ensuring accurate gene transcription and spliceosome assembly. Disruptions in PRPF8 function are linked to a variety of cancers, as mutations in this gene can induce abnormal splicing events that contribute to tumorigenesis, metastasis, and drug resistance. This review provides an in-depth analysis of the mechanisms by which PRPF8 regulates tumorigenesis through AS, exploring its role in diverse cancer types, including breast, liver, myeloid, and colorectal cancers. Furthermore, we examine the molecular pathways associated with PRPF8 dysregulation and their impact on cancer progression. We also discuss the emerging potential of targeting PRPF8 in cancer therapy, highlighting challenges in drug development. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)

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