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Current Issues in Molecular Biology

Current Issues in Molecular Biology is an international, scientific, peer-reviewed, open access journal on molecular biology, published monthly online by MDPI (from Volume 43 Issue 1-2021).

Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
High Visibility: indexed within Scopus, SCIE (Web of Science), PMC, PubMed, Embase, CAPlus / SciFinder, FSTA, AGRIS, and other databases.
Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 17.8 days after submission; acceptance to publication is undertaken in 2.7 days (median values for papers published in this journal in the first half of 2025).
Recognition of Reviewers: APC discount vouchers, optional signed peer review, and reviewer names are published annually in the journal.

Impact Factor: 3.0 (2024); 5-Year Impact Factor: 3.2 (2024)

Imprint Information Journal Flyer Open Access ISSN: 1467-3045

Latest Articles

21 pages, 1881 KB

Open AccessReview

Tumor Immune Microenvironment and Checkpoint Inhibition in Clear Cell Ovarian Carcinoma: Bridging Tumor Biology and Clinical Application in Immunotherapy

by Fulvio Borella, Giulia Capella, Stefano Cosma, Niccolò Gallio, Federica Gavello, Alberto Revelli, Domenico Ferraioli, Jessica Cusato, Isabella Castellano, Paola Cassoni and Luca Bertero

Curr. Issues Mol. Biol. 2025, 47(9), 726; https://doi.org/10.3390/cimb47090726 - 5 Sep 2025

Clear cell ovarian carcinoma is a rare and aggressive histologic subtype of epithelial ovarian cancer, characterized by a chemoresistant phenotype and distinct immunogenomic features. Despite early-phase trials showing a limited response to immune checkpoint inhibitors (ICIs), emerging evidence reveals a biologically diverse tumor [...] Read more.

Clear cell ovarian carcinoma is a rare and aggressive histologic subtype of epithelial ovarian cancer, characterized by a chemoresistant phenotype and distinct immunogenomic features. Despite early-phase trials showing a limited response to immune checkpoint inhibitors (ICIs), emerging evidence reveals a biologically diverse tumor immune microenvironment, with implications for the efficacy of immunotherapies. Preclinical studies highlight paradoxical associations between immune infiltration and prognosis, as well as genomic drivers—including KRAS, MYC, PI3KCA, TP53, PTEN, and ARID1A—that shape immune evasion and checkpoint ligand expression. Clinically, ICI monotherapy yields modest benefit, while combination regimens—particularly dual checkpoint blockade and targeted co-inhibition—offer improved outcomes. Biomarkers such as PD-L1 CPS ≥ 1%, ARID1A mutations, elevated tumor mutational burden, and PIK3CA alterations emerge as promising predictors of therapeutic response. This review integrates current preclinical and clinical data to propose a precision immunotherapy framework tailored to the immunogenomic landscape of clear cell ovarian carcinoma. Full article

(This article belongs to the Special Issue The Molecular Basis of Immunotherapy in Cancer Treatment)

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20 pages, 1543 KB

Open AccessArticle

The Regulation of Catecholamine Biosynthesis by the Gas Transmitters Carbon Monoxide and Hydrogen Sulfide

by Robert Dingley, Cameron Hourtovenko, James Lee, Sujeenthar Tharmalingam and T. C. Tai

Curr. Issues Mol. Biol. 2025, 47(9), 725; https://doi.org/10.3390/cimb47090725 - 5 Sep 2025

The gas transmitters nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H₂S) play important roles in physiological regulation, including adrenal function. Among them, only NO has been directly implicated in controlling catecholamine biosynthesis. This study examined whether CO and H [...] Read more.

The gas transmitters nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H₂S) play important roles in physiological regulation, including adrenal function. Among them, only NO has been directly implicated in controlling catecholamine biosynthesis. This study examined whether CO and H₂S exert similar effects by treating PC12 cells with a CO donor (CORM-2) or an H₂S donor (NaHS), with or without glucocorticoid stimulation. Gene expression of tyrosine hydroxylase (Th), dopamine β-hydroxylase (Dbh), and phenylethanolamine N-methyltransferase (Pnmt) was assessed by RT-qPCR, and catecholamine release was measured by ELISA. We found that exogenous CO decreased Th and Dbh expression, attenuated glucocorticoid-induced upregulation of catecholamine biosynthesis genes, and differentially modulated dopamine and norepinephrine release. In contrast, exogenous H₂S treatment had no significant effect. These findings identify CO as a novel regulator of catecholamine biosynthesis and highlight important differences among gas transmitters in stress-related signaling. Full article

(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)

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42 pages, 1227 KB

Open AccessReview

Microbial Metabolomes in Alzheimer’s Disease: From Pathogenesis to Therapeutic Potential

by Alejandro Borrego-Ruiz and Juan J. Borrego

Curr. Issues Mol. Biol. 2025, 47(9), 724; https://doi.org/10.3390/cimb47090724 - 5 Sep 2025

Background: Accumulating evidence underscores the potential role of the gut microbiome in the pathogenesis of Alzheimer’s disease, but much remains to be clarified. This review examines current evidence linking gut microbiome dysbiosis to Alzheimer’s disease, focusing on microbial metabolomes and their mechanistic role, [...] Read more.

Background: Accumulating evidence underscores the potential role of the gut microbiome in the pathogenesis of Alzheimer’s disease, but much remains to be clarified. This review examines current evidence linking gut microbiome dysbiosis to Alzheimer’s disease, focusing on microbial metabolomes and their mechanistic role, as well as on the potential of therapeutic approaches targeting the gut microbiome. Methods: A narrative, non-systematic examination of the literature was conducted to provide a comprehensive overview of the subject under examination. Database searches were performed in PubMed, Scopus, and Web of Science between June and July 2025. Results: Alzheimer’s disease is linked to reduced gut microbial diversity and altered bacterial taxa. Gut microbiome shifts correlate with inflammation and may drive Alzheimer’s disease progression via the microbiota–gut–brain axis. Microbial amyloids and bacterial products can cross both the intestinal and blood–brain barrier, triggering neuroinflammation and promoting amyloid and tau pathologies. Short-chain fatty acids produced by the gut microbiome regulate neuroinflammation, lipid metabolism, and gene expression, impacting Alzheimer’s disease pathology. Therapeutics targeting the gut microbiome, including probiotics, prebiotics, and fecal microbiota transplantation, show promise in modulating neuroinflammation, reducing amyloid and tau pathology, and improving cognitive function in Alzheimer’s disease. Conclusions: The gut microbiome significantly influences Alzheimer’s disease pathogenesis, and its modulation offers potential to slow progression. However, further research is required to validate effective clinical interventions. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Gut Microbiota in Health, Immunity and Disease)

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43 pages, 4194 KB

Open AccessReview

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

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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14 pages, 1378 KB

Open AccessArticle

A Liposomal Formulation Enhances the Anti-Senescence Properties of Nicotinamide Adenine-Dinucleotide (NAD⁺) in Endothelial Cells and Keratinocytes

by Stefano Ministrini, Luca Liberale, Hanns-Eberhard Erle, Giuseppe Percoco, Ali Tfayli, Ali Assi, Ivan Kapitonov, Isabel Greiner and Giovanni Guido Camici

Curr. Issues Mol. Biol. 2025, 47(9), 722; https://doi.org/10.3390/cimb47090722 - 5 Sep 2025

Nicotinamide adenine-dinucleotide (NAD⁺) supplementation is a promising strategy to delay cellular aging in different areas, including cosmetic dermatology. However, low bioavailability and stability of NAD⁺ formulations are the main factors limiting its effectiveness as an anti-aging treatment. In light of [...] Read more.

Nicotinamide adenine-dinucleotide (NAD⁺) supplementation is a promising strategy to delay cellular aging in different areas, including cosmetic dermatology. However, low bioavailability and stability of NAD⁺ formulations are the main factors limiting its effectiveness as an anti-aging treatment. In light of the above, a liposomal formulation of NAD⁺ (LF-NAD⁺) was tested in this study and compared to NAD⁺ alone in primary human aortic endothelial cells (HAECs) and primary human epidermal keratinocytes (HEKas). Intracellular NAD⁺ was measured using a colorimetric assay. Cell survival was derived from lactate dehydrogenase release in supernatants. Cell senescence was measured by senescence-associated β-galactosidase staining. Molecular mechanisms underlying the reported effects were analyzed by Western blot. Skin penetration of NAD⁺ was measured ex vivo in skin explants, using infrared spectroscopy. Compared to control NAD⁺ alone, the LF-NAD⁺ formulation increased the intracellular NAD⁺ content and cell survival in HAECs, but not in HEKas. Instead, a significant reduction in the number of senescent cells was observed in both HAECs and HEKas. LF-NAD⁺ treatment was associated with a reduced expression of p16 in both HAECs and HEKas, and to a significant reduction in p21 in HEKas alone. Finally, LF-NAD⁺ increases the skin penetration of the active substance NAD⁺ by 30% compared to the application of NAD⁺ alone. LF-NAD⁺, enhances the anti-aging effects of NAD⁺ on vascular and skin cells. Such in vitro findings might indicate a potential anti-aging role in the microcirculation and in the epidermidis. Full article

(This article belongs to the Special Issue Exploring Molecular Pathways in Skin Health and Diseases)

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14 pages, 491 KB

Open AccessReview

Neurodevelopmental Impact of Maternal Immune Activation and Autoimmune Disorders, Environmental Toxicants and Folate Metabolism on Autism Spectrum Disorder

by George Ayoub

Curr. Issues Mol. Biol. 2025, 47(9), 721; https://doi.org/10.3390/cimb47090721 - 4 Sep 2025

Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by deficits in social communication, repetitive behaviors, and sensory sensitivities. While genetic factors contribute significantly to ASD risk, a growing body of evidence implicates environmental exposures and immune-mediated mechanisms in the etiology and [...] Read more.

Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by deficits in social communication, repetitive behaviors, and sensory sensitivities. While genetic factors contribute significantly to ASD risk, a growing body of evidence implicates environmental exposures and immune-mediated mechanisms in the etiology and severity of ASD. This review synthesizes peer-reviewed findings on (1) maternal immune activation, (2) environmental toxicant co-exposures, (3) maternal autoimmune disease, and (4) cerebral folate deficiency (via folate receptor alpha autoantibodies), detailing their mechanistic contributions to core and associated ASD symptoms. Collectively, these findings illuminate converging neuroimmune and metabolic pathways that, when disrupted in utero, substantially alter the developmental trajectory of the brain and increase the likelihood of ASD. Such interruptions leading to developmental changes can trigger immune activation from environmental sources of infection and pollution, with these triggers compounded in cases of autoimmune disease or cerebral folate deficiency. Understanding these mechanisms provides a foundation for early identification, stratified risk assessment, and the development of targeted prenatal interventions. Thus, a lesson we learn from autism is that neurodevelopmental disorders should be understood as the product of combined genetic vulnerabilities and modifiable prenatal and postnatal influences. Further exploration of this framework will open paths for precision intervention and prevention. Full article

(This article belongs to the Special Issue Mental Disorder: Focus on Pathogenesis to Treatment)

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12 pages, 2789 KB

Open AccessArticle

Mechanistic Insights into Vorinostat as a Repositioned Modulator of TACE-Mediated TNF-α Signaling via MAPK and NFκB Pathways

by Jinyoung Park, Muhammad Yasir, Jongseon Choe, Jin-Hee Han, Eun-Taek Han, Won Sun Park and Wanjoo Chun

Curr. Issues Mol. Biol. 2025, 47(9), 720; https://doi.org/10.3390/cimb47090720 - 4 Sep 2025

Vorinostat, an FDA-approved histone deacetylase inhibitor, was evaluated for its potential anti-inflammatory activity through modulation of TACE (ADAM17)-mediated TNF-α signaling. The study was conducted using LPS-stimulated RAW264.7 macrophages. TACE enzymatic activity was assessed by a fluorogenic assay, TNF-α release was measured by ELISA, [...] Read more.

Vorinostat, an FDA-approved histone deacetylase inhibitor, was evaluated for its potential anti-inflammatory activity through modulation of TACE (ADAM17)-mediated TNF-α signaling. The study was conducted using LPS-stimulated RAW264.7 macrophages. TACE enzymatic activity was assessed by a fluorogenic assay, TNF-α release was measured by ELISA, and phosphorylation of MAPKs and NFκB signaling proteins was examined by a western blot. Molecular docking was performed using GNINA to evaluate binding affinity to ERK. Vorinostat was found to modestly inhibit TACE enzymatic activity in vitro, while significantly suppressing TNF-α secretion in cells, comparable to the selective TACE inhibitor BMS-561392. A concentration-dependent reduction in phosphorylated IκB and NFκB was observed, along with selective inhibition of ERK phosphorylation. Docking studies indicated a stable, albeit weaker, binding of vorinostat to ERK compared to reference ERK inhibitors. These findings suggest that vorinostat suppresses TNF-α production primarily through indirect mechanisms involving ERK and NF-κB signaling pathways, rather than by direct TACE inhibition. The repositioning of vorinostat as a modulator of inflammatory signaling is supported, offering potential therapeutic value in inflammatory disorders. Full article

(This article belongs to the Section Molecular Medicine)

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25 pages, 2088 KB

Open AccessArticle

Evaluation of the Antihyperalgesic Potential of Morus alba, Angelica archangelica, Valeriana officinalis, and Passiflora incarnata in Alloxan-Induced Diabetic Neuropathy in Rats

by Felicia Suciu, Ciprian Pușcașu, Dragos Paul Mihai, Anca Ungurianu, Corina Andrei, Robert Viorel Ancuceanu, Cerasela Elena Gîrd, Anne-Marie Ciobanu, Nicoleta Mirela Blebea, Violeta Popovici, Cristina Isabel Viorica Ghiță and Simona Negres

Curr. Issues Mol. Biol. 2025, 47(9), 719; https://doi.org/10.3390/cimb47090719 - 4 Sep 2025

Diabetic neuropathy (DN) is one of the most prevalent complications of diabetes mellitus, affecting a substantial proportion of patients and contributing to progressive sensorimotor dysfunction. Despite its clinical significance, available treatments are often insufficient and associated with undesirable effects. This study aims to [...] Read more.

Diabetic neuropathy (DN) is one of the most prevalent complications of diabetes mellitus, affecting a substantial proportion of patients and contributing to progressive sensorimotor dysfunction. Despite its clinical significance, available treatments are often insufficient and associated with undesirable effects. This study aims to evaluate the potential of Morus alba (MA), Angelica archangelica (AA), Valeriana officinalis (VO), and Passiflora incarnata (PI) extracts in ameliorating nociceptive alterations and inflammatory markers in the alloxan-induced diabetic rat model. Male Wistar rats with alloxan-induced DN received oral administration of the plant extracts (200 mg/kg/day) or gabapentin (100 mg/kg/day) for 15 days, the dosage regimen being established based on prior efficacy data in preclinical neuropathy models. Behavioral assessments of thermal and mechanical hypersensitivity were conducted using hot plate, tail withdrawal, von Frey, and Randall–Sellito tests. Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were quantified in brain and liver homogenates to evaluate neuro-inflammatory responses. All plant extracts produced significant improvements in nociceptive thresholds compared to diabetic control, with the most marked effects observed for MA extract. Pro-inflammatory cytokine levels were significantly reduced in all treatment groups, with MA and AA extracts inducing the most significant reductions in TNF-α and IL-6 concentrations. Computational target prediction and molecular docking analyses revealed that key phytochemicals from the plant extracts may exert antihyperalgesic effects through multi-target modulation, notably via interactions with AAK1, a kinase involved in neuropathic pain signaling. The investigated plant extracts displayed significant antihyperalgesic and anti-inflammatory activities in a rat model of DN. Among them, MA extract revealed the most consistent therapeutic profile, supporting its potential role as a strategy for managing DN. Full article

(This article belongs to the Special Issue Natural Products as Potential Sources of Antidiabetic Compounds, 2nd Edition)

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13 pages, 1448 KB

Open AccessReview

A Review of Syndromic Forms of Obesity: Genetic Etiology, Clinical Features, and Molecular Diagnosis

by Anam Farzand, Mohd Adzim Khalil Rohin, Sana Javaid Awan, Zubair Sharif, Adnan Yaseen and Abdul Momin Rizwan Ahmad

Curr. Issues Mol. Biol. 2025, 47(9), 718; https://doi.org/10.3390/cimb47090718 - 3 Sep 2025

Background: Syndromic forms of obesity are uncommon, complicated illnesses that include early-onset obesity along with other clinical characteristics such as organ-specific abnormalities, dysmorphic symptoms, and intellectual incapacity. These syndromes frequently have a strong genetic foundation, involving copy number variations, monogenic mutations, and chromosomal [...] Read more.

Background: Syndromic forms of obesity are uncommon, complicated illnesses that include early-onset obesity along with other clinical characteristics such as organ-specific abnormalities, dysmorphic symptoms, and intellectual incapacity. These syndromes frequently have a strong genetic foundation, involving copy number variations, monogenic mutations, and chromosomal abnormalities. Methods: Using terms like “syndromic obesity,” “genetic diagnosis,” and “monogenic obesity,” a comprehensive literature search was conducted to find articles published between 2000 and 2025 in PubMed, Scopus, and Web of Science. Peer-reviewed research addressing the clinical, molecular, or genetic aspects of syndromic obesity were among the inclusion criteria. Conference abstracts, non-English publications, and research without genetic validation were among the exclusion criteria. The whole genetic, clinical, diagnostic, and therapeutic domains were thematically synthesized to create a thorough, fact-based story. Research using chromosomal microarray analysis (CMA), whole-exome sequencing (WES), next-generation sequencing (NGS), and new long-read sequencing platforms was highlighted. Results: Despite the fact that molecular diagnostics, especially NGS and CMA, have made tremendous progress in identifying pathogenic variants, between 30 and 40 percent of instances of syndromic obesity are still genetically unexplained. One significant issue is the variation in phenotype across people with the same mutation, which suggests the impact of environmental modifiers and epigenetic variables. In addition, differences in access to genetic testing, particularly in areas with limited resources, can make it difficult to diagnose patients in a timely manner. Additionally, recent research emphasizes the possible contribution of gene–environment interactions, gut microbiota, and multi-omic integration to modifying disease expression. Conclusions: Syndromic obesity is still poorly understood in a variety of groups despite significant advancements in technology. Multi-layered genomic investigations, functional genomic integration, and standardized diagnostic frameworks are necessary to close existing gaps. The development of tailored treatment plans, such as gene editing and focused pharmaceutical therapies as well as fair access to cutting-edge diagnostics are essential to improving outcomes for people with syndromic obesity. Full article

(This article belongs to the Special Issue Mechanisms and Pathophysiology of Obesity)

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15 pages, 2810 KB

Open AccessArticle

The Anti-Tumor and Bortezomib-Sensitizing Effects of Apigenin in Multiple Myeloma

by Ye Chen, Lan Wu, Siyu Wang, Huihao Chen, Miaojun Chen, Yanfen Huang and Bin Ding

Curr. Issues Mol. Biol. 2025, 47(9), 717; https://doi.org/10.3390/cimb47090717 - 3 Sep 2025

Multiple myeloma (MM) is a kind of plasma cell neoplasm, accounting for approximately 10% of hematologic malignancies, with a high mortality rate. Apigenin (APG), a flavonoid, has been reported to have antiviral, antibacterial, antioxidant, and anticancer properties. However, the impact of APG on [...] Read more.

Multiple myeloma (MM) is a kind of plasma cell neoplasm, accounting for approximately 10% of hematologic malignancies, with a high mortality rate. Apigenin (APG), a flavonoid, has been reported to have antiviral, antibacterial, antioxidant, and anticancer properties. However, the impact of APG on MM and bortezomib (BTZ) sensitization has not been investigated. The effects of APG on the proliferation, cell cycle, apoptosis, and oxidative stress of RPMI-8226 and U266 cells were investigated using CCK-8 assay, crystal violet staining, flow cytometry, Western blot, and PCR. It was observed that APG treatment increased the G1 phase cells, by which the expression of P21 increased, and the expression of CDK2 and Cyclin D1 decreased. Even though Necrostatin-1 (a potent necroptosis inhibitor) and Fer-1 (a ferroptosis inhibitor) could attenuate the effect of APG, the effect of Z-VAD-FMK (a pan-caspase inhibitor) was more significant. APG treatment increased the transcription of P53 and BAX, and the level of cleaved-PARP1 and cleaved-Caspase 3 in two MM cell strains. In addition, the APG application could dose-dependently increase the ROS, MDA, and GSSH levels, and decrease the GSH level in both cell strains, by which the transcription of GCLC, NQO1, GSTM2, NRF2, and GPX4 were attenuated. Finally, APG enhances the inhibitory effect of BTZ on MM cell growth. This study provides a potential therapeutic approach of APG on MM. Full article

(This article belongs to the Section Molecular Pharmacology)

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44 pages, 4218 KB

Open AccessReview

Revisiting Curcumin in Cancer Therapy: Recent Insights into Molecular Mechanisms, Nanoformulations, and Synergistic Combinations

by Khadija Akter, Kainat Gul and Sohail Mumtaz

Curr. Issues Mol. Biol. 2025, 47(9), 716; https://doi.org/10.3390/cimb47090716 - 3 Sep 2025

Curcumin has been extensively investigated as an anticancer agent, yet its clinical application remains constrained by low bioavailability, incomplete mechanistic understanding, and limited therapeutic optimization. In light of growing resistance to conventional chemotherapies and the demand for safer, multi-targeted agents, this review revisits [...] Read more.

Curcumin has been extensively investigated as an anticancer agent, yet its clinical application remains constrained by low bioavailability, incomplete mechanistic understanding, and limited therapeutic optimization. In light of growing resistance to conventional chemotherapies and the demand for safer, multi-targeted agents, this review revisits curcumin with a contemporary lens. We critically evaluate the literature published since 2020, focusing on newly elucidated molecular mechanisms by which curcumin regulates tumor progression, including modulation of oncogenic signaling pathways (Wnt/β-catenin, PI3K/Akt/mTOR, JAK/STAT, and MAPK), induction of ferroptosis, and epigenetic reprogramming. A particular emphasis is placed on recent advances in nanoformulation strategies that enhance curcumin’s pharmacokinetic profile and target-specific delivery. Furthermore, the emerging paradigm of combination therapy is explored, where curcumin acts synergistically with chemotherapeutics and phytochemicals to overcome drug resistance and potentiate anticancer efficacy. This review identifies key knowledge gaps, such as inconsistent clinical translation and the underexplored interplay between nanocurcumin systems and immune modulation, outlining directions for future translational research. Full article

(This article belongs to the Special Issue Natural Compounds: An Adjuvant Strategy in Cancer Management)

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13 pages, 526 KB

Open AccessReview

Metformin as a Disease-Modifying Agent in Autosomal Dominant Polycystic Kidney Disease: A Systematic Review of Preclinical and Clinical Evidence

by Aleksandra Maciejczyk and Mariusz Niemczyk

Curr. Issues Mol. Biol. 2025, 47(9), 715; https://doi.org/10.3390/cimb47090715 - 3 Sep 2025

Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited kidney disorder marked by cyst growth and progressive renal failure. This systematic review aims to summarize current preclinical and clinical evidence on the potential role of metformin in ADPKD, focusing on its effects [...] Read more.

Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited kidney disorder marked by cyst growth and progressive renal failure. This systematic review aims to summarize current preclinical and clinical evidence on the potential role of metformin in ADPKD, focusing on its effects on glucose metabolism, kidney function, inflammation, and survival. A comprehensive search was conducted in PubMed and Google Scholar up to June 2025, following PRISMA guidelines. Forty-two articles met the inclusion criteria and were analyzed. Included studies examined metformin use in ADPKD patients or models and reported outcomes such as renal function, cyst growth, metabolic markers, and mortality. In preclinical studies, it reduced cyst formation, improved kidney structure, and decreased inflammation. Clinical studies confirmed its safety and suggested benefits in slowing kidney function decline, especially in early-stage ADPKD. Metformin may be a promising supportive therapy in ADPKD due to its metabolic and anti-inflammatory effects. Full article

(This article belongs to the Collection Molecular Mechanisms in Human Diseases)

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13 pages, 1454 KB

Open AccessArticle

The TOX2 Gene Is Responsible for Conidiation and Full Virulence in Fusarium pseudograminearum

by Sen Han, Shaobo Zhao, Yajiao Wang, Qiusheng Li, Mengwei Sun, Lingxiao Kong, Xianghong Chen, Jianhai Gao and Yuxing Wu

Curr. Issues Mol. Biol. 2025, 47(9), 714; https://doi.org/10.3390/cimb47090714 - 2 Sep 2025

Fusarium crown rot, a widespread and destructive disease affecting cereal crops (particularly wheat and barley), is primarily caused by the soil-borne fungal pathogen Fusarium pseudograminearum. Secondary metabolites (SMs) play a crucial role in colonization and host tissue invasion by pathogenic fungi. In [...] Read more.

Fusarium crown rot, a widespread and destructive disease affecting cereal crops (particularly wheat and barley), is primarily caused by the soil-borne fungal pathogen Fusarium pseudograminearum. Secondary metabolites (SMs) play a crucial role in colonization and host tissue invasion by pathogenic fungi. In this study, we investigated the functional role of FpTox2, a secondary metabolite-related gene in F. pseudograminearum. An FpTox2 deletion mutant exhibited significantly reduced radial growth compared to wild-type F. pseudograminearum. Notably, the mutant strain completely lost conidiation capacity under induced conditions. Furthermore, although it showed decreased sensitivity to the cell membrane inhibitor sodium dodecyl sulfate (SDS), the mutant demonstrated enhanced susceptibility to NaCl, a metal ion stressor. Most importantly, the pathogen’s virulence was markedly attenuated in wheat stem base infections following FpTox2 deletion, and we demonstrated that FpTox2 regulates pathogen virulence by influencing deoxynivalenol production. In conclusion, FpTox2 is crucial for vegetative growth, asexual development, abiotic stress responses, and full virulence in F. pseudograminearum. Full article

(This article belongs to the Section Molecular Microbiology)

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19 pages, 733 KB

Open AccessReview

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

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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24 pages, 7654 KB

Open AccessArticle

PSMB9 Orchestrates Tumor Immune Landscape and Serves as a Potent Biomarker for Prognosis and T Cell-Based Immunotherapy Response

by Xinran Ma, Qi Zhu, Zhiqiang Wu and Weidong Han

Curr. Issues Mol. Biol. 2025, 47(9), 712; https://doi.org/10.3390/cimb47090712 - 1 Sep 2025

Proteasome subunit beta type-9 (PSMB9), a member of the proteasome beta subunit family, encodes the pivotal β1i component of the immunoproteasome. PSMB9 plays a crucial role in antigen processing and presentation; however, its comprehensive role in orchestrating a tumor-immune landscape and regulating the [...] Read more.

Proteasome subunit beta type-9 (PSMB9), a member of the proteasome beta subunit family, encodes the pivotal β1i component of the immunoproteasome. PSMB9 plays a crucial role in antigen processing and presentation; however, its comprehensive role in orchestrating a tumor-immune landscape and regulating the anti-tumor immune responses remains unexplored. Here we investigated the context-dependent functions of PSMB9 by integrating multi-omics data from The Cancer Genome Atlas, Genotype-Tissue Expression database, Human Protein Atlas, Tumor Immunotherapy Gene Expression Resource, and multiple other databases. Moreover, we explored the predictive value of PSMB9 in multiple immunotherapy cohorts and investigated its functional relevance in CAR-T therapy using genome-scale CRISPR/Cas9 screening, gene knockout cell line in vitro, and clinical cohort validation. We found widespread dysregulation in PSMB9 across cancers, predominantly upregulated in most malignancies and associated with advanced pathological stages in specific contexts. PSMB9 was also broadly and negatively correlated with tumor stemness indices. Crucially, PSMB9 expression was robustly linked to anti-tumor immunity by being significantly correlated with immune-pathway activation (e.g., IFN response, cytokine signaling), immune regulatory and immune checkpoint gene expression, and enhanced infiltration of T cells across nearly all tumor types. Consequently, elevated PSMB9 predicted superior response to immune checkpoint inhibitors in multiple cohorts, showing comparable predictive power to established predictive signatures. Furthermore, CRISPR/Cas9 screening identified PSMB9 loss as a novel mechanism of resistance to CD19 CAR T cell therapy, with PSMB9-deficient tumor cells exhibiting a survival advantage under CAR-T pressure, supported by trends in clinical CAR-T outcomes. Our study uncovers PSMB9 as a previously unrecognized critical regulator of the tumor immune landscape in a pan-cancer scope, whose expression orchestrates key immune processes within the tumor microenvironment and serves as a potent biomarker for patient prognosis. Critically, we first established PSMB9 as a novel prognostic indicator for both checkpoint blockade and CAR-T cell therapies, highlighting its dual role as a crucial immune modulator and a promising biomarker for guiding T cell-based immunotherapy strategies across diverse human cancers. Full article

(This article belongs to the Section Molecular Medicine)

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15 pages, 784 KB

Open AccessReview

Smart Red Blood Cell Carriers: A Nanotechnological Approach to Cancer Drug Delivery

by Ioannis Tsamesidis, Georgios Dryllis, Sotirios P. Fortis, Andreas Sphicas, Vasiliki Konstantinidou, Maria Chatzidimitriou, Stella Mitka, Maria Trapali, Petros Skepastianos, Anastasios G. Kriebardis and Ilias Pessach

Curr. Issues Mol. Biol. 2025, 47(9), 711; https://doi.org/10.3390/cimb47090711 - 1 Sep 2025

The efficient and targeted delivery of pharmaceutical substances remains a major challenge in modern therapeutics. Traditional drug delivery systems often suffer from limited bioavailability, rapid clearance, and off-target effects. Red blood cells (erythrocytes), due to their long circulation time, biocompatibility, and immune-evasive properties, [...] Read more.

The efficient and targeted delivery of pharmaceutical substances remains a major challenge in modern therapeutics. Traditional drug delivery systems often suffer from limited bioavailability, rapid clearance, and off-target effects. Red blood cells (erythrocytes), due to their long circulation time, biocompatibility, and immune-evasive properties, have emerged as promising carriers in the development of novel nanotechnology-based drug delivery platforms.A comprehensive literature review was conducted, analyzing recent studies on erythrocyte membrane-coated nanoparticles, their interactions with loaded therapeutic agents, and their performance in vitro and in vivo. Special focus was given to applications in chemotherapy, photodynamic therapy (PDT), photothermal therapy (PTT), and immunotherapy. Erythrocyte-based nanocarriers demonstrated improved circulation times, reduced immune clearance, and enhanced targeting capabilities compared to traditional nanoparticles. Encapsulation of nanoparticles within erythrocyte membranes preserved the functional integrity of the carrier while minimizing systemic toxicity. However, challenges such as membrane stability, hemocompatibility, and the potential for nanoparticle-induced hemoglobin dysfunction were identified as areas requiring further research. In conclusion, erythrocyte membrane-coated nanoparticles represent a unique and promising strategy for drug delivery, combining the natural advantages of red blood cells with the versatility of nanotechnology. Full article

(This article belongs to the Special Issue The Contribution and Application of Molecular Biology in the Applied Biosciences—Focusing on Medicine, Biomaterials and Tissue Engineering Fields, 2nd Edition)

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37 pages, 2146 KB

Open AccessReview

The Central Nervous System Modulatory Activities of N-Acetylcysteine: A Synthesis of Two Decades of Evidence

by Desislava Ivanova Cherneva, Gabriela Kehayova, Simeonka Dimitrova and Stela Dragomanova

Curr. Issues Mol. Biol. 2025, 47(9), 710; https://doi.org/10.3390/cimb47090710 - 1 Sep 2025

N-acetylcysteine (NAC) has garnered increasing interest for its neurotherapeutic capabilities beyond its recognized functions as a mucolytic agent and an antidote for acetaminophen toxicity. This review consolidates findings from both preclinical and clinical studies to investigate NAC’s diverse modulatory effects on the central [...] Read more.

N-acetylcysteine (NAC) has garnered increasing interest for its neurotherapeutic capabilities beyond its recognized functions as a mucolytic agent and an antidote for acetaminophen toxicity. This review consolidates findings from both preclinical and clinical studies to investigate NAC’s diverse modulatory effects on the central nervous system (CNS). NAC primarily functions as an antioxidant by replenishing glutathione and mitigating oxidative stress; however, it produces glutathione-independent effects through the modulation of mitochondrial redox systems, ferroptosis, and the Nrf2-ARE signaling pathway. It plays a significant role in neuroinflammatory processes by inhibiting the production of cytokines, the expression of iNOS, and the activation of microglia. Furthermore, NAC affects various neurotransmitter systems—including glutamatergic, dopaminergic, GABAergic, serotonergic, cholinergic, and adrenergic pathways—by modulating synaptic transmission, receptor activity, and transporter functionality. It promotes neuroprotection through the enhancement of neurotrophic factors, the preservation of mitochondrial integrity, and the upregulation of survival signaling pathways. Recent evidence also emphasizes NAC’s role in gene expression and the regulation of cortisol levels. The extensive range of NAC’s neurobiological effects highlights its therapeutic potential in treating neurodegenerative and neuropsychiatric disorders. Nevertheless, the variability in clinical outcomes indicates a pressing need for more focused, mechanism-based research. Full article

(This article belongs to the Section Molecular Pharmacology)

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29 pages, 4063 KB

Open AccessReview

Synergism of Synthetic Sulfonamides and Natural Antioxidants for the Management of Diabetes Mellitus Associated with Oxidative Stress

by Ancuța Dinu (Iacob), Luminita-Georgeta Confederat, Ionut Dragostin, Ionela Daniela Morariu, Dana Tutunaru and Oana-Maria Dragostin

Curr. Issues Mol. Biol. 2025, 47(9), 709; https://doi.org/10.3390/cimb47090709 - 1 Sep 2025

In the context of expanding research on the development of compounds with multiple therapeutic actions, this study aims to consolidate findings from the last decade on new synthetic sulfonamide therapies for managing type 2 diabetes mellitus (T2DM) associated with oxidative stress (OS). The [...] Read more.

In the context of expanding research on the development of compounds with multiple therapeutic actions, this study aims to consolidate findings from the last decade on new synthetic sulfonamide therapies for managing type 2 diabetes mellitus (T2DM) associated with oxidative stress (OS). The novelty of this synthesis study lies in the synergistic approach of antidiabetic molecular targets with those against oxidative stress, having the sulfonylurea class as a common point. By utilizing international databases, we identified and selected conclusive studies for this review. Promising results have been achieved through dual therapies that combine antioxidants (such as sesame oil, naringin, alpha-lipoic acid, resveratrol, and quercetin) with sulfonylureas (including glipizide, glibenclamide, gliclazide, and glimepiride). Additionally, triple therapies that associated sulfonylureas with other classes of antidiabetic medications have also shown encouraging outcomes. These findings are supported by in vivo tests conducted on experimental laboratory models as well as on human subjects. These recent advancements in synthetic sulfonamide research point to a promising future in diabetes management, especially considering the dual functionalities demonstrated by in vivo studies—specifically, their antidiabetic and antioxidant effects. Moreover, the synergy between sulfonamides and other antioxidant agents represents a beneficial strategy for optimizing future chemical structures, potentially allowing for their integration into personalized treatments aimed at combating T2DM. Full article

(This article belongs to the Special Issue Advances in Molecular Therapies and Disease Associations in Diabetes)

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18 pages, 2265 KB

Open AccessArticle

Krill Oil Mitigates Cisplatin-Induced Ovarian Toxicity via Attenuation of Oxidative Stress and Inflammatory Pathways

by Erson Aksu and Oytun Erbas

Curr. Issues Mol. Biol. 2025, 47(9), 708; https://doi.org/10.3390/cimb47090708 - 1 Sep 2025

Cisplatin remains a cornerstone chemotherapeutic agent; however, its off-target gonadotoxicity poses a significant risk for premature ovarian failure (POF) and infertility in young women. Strategies to preserve ovarian function during chemotherapy are critically needed. To investigate the protective effects of krill oil supplementation [...] Read more.

Cisplatin remains a cornerstone chemotherapeutic agent; however, its off-target gonadotoxicity poses a significant risk for premature ovarian failure (POF) and infertility in young women. Strategies to preserve ovarian function during chemotherapy are critically needed. To investigate the protective effects of krill oil supplementation against cisplatin-induced ovarian damage in a rat model, with a focus on oxidative stress, inflammation, follicular dynamics, and stromal fibrosis. Twenty-one adult female Wistar albino rats were randomized into three groups: control, cisplatin-treated, and cisplatin + krill oil-treated. Ovarian toxicity was induced via intraperitoneal injection of cisplatin (2.5 mg/kg, twice weekly for four weeks). Krill oil (4 mL/kg/day) was administered orally during the same period. Ovarian histopathology, follicle counts (primordial, primary, secondary, tertiary), stromal fibrosis, and biochemical markers, including plasma anti-Müllerian hormone (AMH), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and ovarian levels of nuclear factor erythroid 2-related factor 2 (Nrf2), Toll-like receptor 4 (TLR4), TNF-α, NOD-like receptor family pyrin domain containing 3 (NLRP3), and IL-1β were evaluated. Cisplatin significantly reduced primordial, primary, secondary, and tertiary follicle counts while increasing stromal fibrosis (p < 0.001). Krill oil co-treatment notably ameliorated follicular depletion—improving follicle counts by 38.16%, 54.74%, 62.5%, 40.43%, respectively—and reduced fibrosis (p = 0.017). Biochemically, cisplatin decreased AMH levels and Nrf2 expression while elevating MDA, TNF-α, TLR4, NLRP3, and IL-1β levels (p < 0.001). Krill oil supplementation restored AMH (p = 0.002) and Nrf2 (p = 0.003) levels, while reducing MDA (p = 0.009), NLRP3 (p < 0.001), ovarian IL-1β (p = 0.005), plasma IL-1β (p < 0.001), TLR4 (p = 0.001), plasma TNF-α (p = 0.001), and ovarian TNF-α (p < 0.001), compared to the cisplatin group. Krill oil exerts significant antioxidant and anti-inflammatory effects, offering a promising strategy to mitigate cisplatin-induced ovarian damage and preserve fertility in young cancer patients. Full article

(This article belongs to the Section Molecular Medicine)

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15 pages, 1484 KB

Open AccessArticle

Effect of Sperm DNA Fragmentation and Chromatin Decondensation on PLCζ Efficacy in Infertile Patients

by Soukaina Azil, Ismail Kaarouch, Debbie Montjean, Marie-Hélène Godin Pagé, Rosalie Cabry, Noureddine Louanjli, Bouchra Ghazi and Moncef Benkhalifa

Curr. Issues Mol. Biol. 2025, 47(9), 707; https://doi.org/10.3390/cimb47090707 - 1 Sep 2025

This study aimed to describe phospholipase C zeta (PLCζ) deficiency from patients who experienced oocyte fertilization failure following intracytoplasmic sperm injection (ICSI) and to investigate the relationship between sperm DNA fragmentation, chromatin decondensation, and PLCζ. A total of 135 patients participated in this [...] Read more.

This study aimed to describe phospholipase C zeta (PLCζ) deficiency from patients who experienced oocyte fertilization failure following intracytoplasmic sperm injection (ICSI) and to investigate the relationship between sperm DNA fragmentation, chromatin decondensation, and PLCζ. A total of 135 patients participated in this study—65 fertile men and 70 infertile patients— and semen samples were obtained to analyze concentration, motility, and morphology. PLCζ protein levels were assessed by immunofluorescence and quantitative techniques, DNA fragmentation by TUNEL essay, and chromatin decondensation by aniline blue staining. The proportion of spermatozoa presenting PLCζ was significantly lower in infertile patients (18.41 ± 18.84%) compared to fertile controls (67.31 ± 13.79%) (p < 0.001). A significant decrease in PLCζ protein levels was observed in infertile patients compared to fertile controls, which was the same for localization patterns for each region (acrosomal, equatorial, and combination of these regions). Significant correlations were also observed between sperm parameters and PLCζ levels, DNA fragmentation, and chromatin decondensation. Furthermore, a statistically significant correlation was detected between the percentage of spermatozoa presenting PLCζ and DNA integrity (p < 0.001). In summary, DNA fragmentation and chromatin decondensation are associated with alterations in the localization patterns and reduced protein levels of PLCζ, which may contribute to total fertilization failure. Full article

(This article belongs to the Collection Molecular Mechanisms in Human Diseases)

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