Journal Description
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 15.8 days after submission; acceptance to publication is undertaken in 2.6 days (median values for papers published in this journal in the second half of 2024).
- Recognition of Reviewers: APC discount vouchers, optional signed peer review, and reviewer names are published annually in the journal.
Impact Factor:
2.8 (2023);
5-Year Impact Factor:
2.9 (2023)
Latest Articles
The Potential Role of sPD-L1 as a Predictive Biomarker in EGFR-Positive Non-Small-Cell Lung Cancer
Curr. Issues Mol. Biol. 2025, 47(1), 45; https://doi.org/10.3390/cimb47010045 (registering DOI) - 11 Jan 2025
Abstract
Background/Objectives: A significant breakthrough in non-small-cell lung cancer (NSCLC) treatment has occurred with the introduction of targeted therapies and immunotherapy. However, not all patients treated with these therapies would respond to treatment, and patients who respond to treatment would acquire resistance at some
[...] Read more.
Background/Objectives: A significant breakthrough in non-small-cell lung cancer (NSCLC) treatment has occurred with the introduction of targeted therapies and immunotherapy. However, not all patients treated with these therapies would respond to treatment, and patients who respond to treatment would acquire resistance at some time point. This is why we need new biomarkers that can predict response to therapy. The aim of this study was to investigate whether soluble programmed cell death-ligand 1 (sPD-L1) could be a predictive biomarker in patients with epidermal growth factor receptor (EGFR)-positive NSCLC. Materials and Methods: Blood samples from 35 patients with EGFR-mutated (EGFRmut) adenocarcinoma who achieved disease control with EGFR tyrosine kinase inhibitor (EGFR TKI) therapy were collected for sPD-L1 analysis. We analyzed sPD-L1 concentrations in 30 healthy middle-aged subjects, as a control population, to determine the reference range. Adenocarcinoma patients were divided into two groups, i.e., a group with low sPD-L1 (≤182.5 ng/L) and a group with high sPD-L1 (>182.5 ng/L). Results: We found that progression-free survival (PFS) was 18 months, 95% CI (11.1–24.9), for patients with low sPD-L1 and 25 months, 95% CI (8.3–41.7), for patients with high sPD-L1. There was no statistically significant difference in PFS between the groups (p = 0.100). Overall survival (OS) was 34.4 months, 95% CI (26.6–42.2), for patients with low sPD-L1 and 84.1 months, 95% CI (50.6–117.6), for patients with high sPD-L1; there was also no statistically significant difference between the groups (p = 0.114). Conclusion: In our study, we found that patients with high sPD-L1 had numerically better PFS and OS, but this has no statistical significance. Further studies with a larger number of patients are needed to evaluate the role of sPD-L1 as a predictive biomarker in patients with EGFRmut NSCLC.
Full article
(This article belongs to the Special Issue Targeting Tumor Microenvironment for Cancer Therapy, 3rd Edition)
►
Show Figures
Open AccessArticle
Notoginsenoside R1 Attenuates H/R Injury in H9c2 Cells by Maintaining Mitochondrial Homeostasis
by
Yuanbo Xu, Piao Wang, Ting Hu, Ke Ning and Yimin Bao
Curr. Issues Mol. Biol. 2025, 47(1), 44; https://doi.org/10.3390/cimb47010044 - 10 Jan 2025
Abstract
Mitochondrial homeostasis is crucial for maintaining cellular energy production and preventing oxidative stress, which is essential for overall cellular function and longevity. Mitochondrial damage and dysfunction often occur concomitantly in myocardial ischemia–reperfusion injury (MIRI). Notoginsenoside R1 (NGR1), a unique saponin from the traditional
[...] Read more.
Mitochondrial homeostasis is crucial for maintaining cellular energy production and preventing oxidative stress, which is essential for overall cellular function and longevity. Mitochondrial damage and dysfunction often occur concomitantly in myocardial ischemia–reperfusion injury (MIRI). Notoginsenoside R1 (NGR1), a unique saponin from the traditional Chinese medicine Panax notoginseng, has been shown to alleviate MIRI in previous studies, though its precise mechanism remains unclear. This study aimed to elucidate the mechanisms of NGR1 in maintaining mitochondrial homeostasis in hypoxia/reoxygenation (H/R) H9c2 cells. The results showed that NGR1 pretreatment effectively increased cell survival rates post-H/R, reduced lactate dehydrogenase (LDH) leakage, and mitigated cell damage. Further investigation into mitochondria revealed that NGR1 alleviated mitochondrial structural damage, improved mitochondrial membrane permeability transition pore (mPTP) persistence, and prevented mitochondrial membrane potential (Δψm) depolarization. Additionally, NGR1 pretreatment enhanced ATP levels, increased the activity of mitochondrial respiratory chain complexes I–V after H/R, and reduced excessive mitochondrial reactive oxygen species (mitoROS) production, thereby protecting mitochondrial function. Further analysis indicated that NGR1 upregulated the expression of mitochondrial biogenesis-related proteins (PGC-1α, Nrf1, Nrf2) and mitochondrial fusion proteins (Opa1, Mfn1, Mfn2), while downregulating mitochondrial fission proteins (Fis1, Drp1) and reducing mitochondrial autophagy (mitophagy) levels, as well as the expression of mitophagy-related proteins (Pink1, Parkin, BNIP3) post-H/R. Therefore, this study showed that NGR1 can maintain mitochondrial homeostasis by regulating mitophagy, mitochondrial fission–fusion dynamics, and mitochondrial biogenesis, thereby alleviating H9c2 cell H/R injury and protecting cardiomyocytes.
Full article
(This article belongs to the Special Issue Pharmacological Activities and Mechanisms of Action of Natural Products)
Open AccessArticle
Acidic Microenvironment Enhances Cisplatin Resistance in Bladder Cancer via Bcl-2 and XIAP
by
Kaede Hiruma, Vladimir Bilim, Akira Kazama, Yuko Shirono, Masaki Murata and Yoshihiko Tomita
Curr. Issues Mol. Biol. 2025, 47(1), 43; https://doi.org/10.3390/cimb47010043 - 10 Jan 2025
Abstract
Cisplatin (CDDP) remains a key drug for patients with advanced bladder cancer (BC), despite the emergence of new therapeutic agents; thus, the identification of factors contributing to CDDP treatment resistance is crucial. As acidity of the tumor microenvironment has been reported to be
[...] Read more.
Cisplatin (CDDP) remains a key drug for patients with advanced bladder cancer (BC), despite the emergence of new therapeutic agents; thus, the identification of factors contributing to CDDP treatment resistance is crucial. As acidity of the tumor microenvironment has been reported to be associated with treatment resistance and poor prognosis across various cancer types, our objectives in this study were to investigate the effects of an acidic environment on BC cells and elucidate the mechanisms behind CDDP resistance. Our findings show that BC cells cultured under acidic conditions developed cisplatin resistance as acidity increased. Notably, CDDP administered to BC cells in a pH 6.0 environment required double the concentration, compared to those in a pH 7.5 environment, to achieve equivalent toxicity. Using chloroquine and navitoclax, we identified the involvement of the Bcl-2 and LC3B pathways in the acquisition of CDDP resistance under acidic conditions. A Western blot analysis revealed that the activations of Bcl-2 and XIAP expression appear to inhibit both apoptotic and autophagic cell death. Taken together, these results suggest that alleviating the acidity of the tumor microenvironment in clinical settings might enhance BC sensitivity to CDDP.
Full article
(This article belongs to the Special Issue Targeting Tumor Microenvironment for Cancer Therapy, 3rd Edition)
►▼
Show Figures
Figure 1
Open AccessCommunication
Plant miRNAs for Improved Gene Regulation in a Wide Range of Human Cancers
by
Maksym Zoziuk, Vittorio Colizzi, Pavlo Krysenko, Maurizio Mattei, Roberta Bernardini, Fabio Massimo Zanzotto, Stefano Marini and Dmitri Koroliouk
Curr. Issues Mol. Biol. 2025, 47(1), 42; https://doi.org/10.3390/cimb47010042 - 9 Jan 2025
Abstract
Determining the relationships between miRNA expression, target genes, and cancer development is critical to cancer research. The possibility of correlating miRNA expression with plant or artificial ones provides prerequisites for cancer treatment. Based on the broad database of human miRNA expression for all
[...] Read more.
Determining the relationships between miRNA expression, target genes, and cancer development is critical to cancer research. The possibility of correlating miRNA expression with plant or artificial ones provides prerequisites for cancer treatment. Based on the broad database of human miRNA expression for all cancer types, we grade human miRNAs by their expression level. The identified deficient miRNAs are compared with their target genes for coincidences in their expression directions. The replacement of human miRNAs is proposed to be implemented, using plant miRNAs closest to the human-deficient ones. Such plant substitutes are identified by analyzing the average complementarity of all human under-expressed miRNAs. It was established that the number of downregulated miRNAs is almost 2.5 times greater than that of upregulated miRNAs. There is no significant correlation between the expression of miRNA and genes, implying many other expression regulation mechanisms exist. Working on the organization of experimental verification of the obtained statistical studies, we present significant regularities that provide grounds for considering some plant microRNAs as possible means of compensating for insufficient expression of regulatory microRNAs in humans and animals in a wide range of oncological diseases.
Full article
(This article belongs to the Special Issue The Significance of Transcription Factors, miRNAs, and lncRNAs in Anticancer Drug Development)
Open AccessArticle
First Report on Microbial-Derived Polydeoxyribonucleotide: A Sustainable and Enhanced Alternative to Salmon-Based Polydeoxyribonucleotide
by
Doobyeong Chae, Sae-Woong Oh, Yoon-Seo Choi, Dae-Jung Kang, Chun-Woong Park, Jongsung Lee and Won-Sang Seo
Curr. Issues Mol. Biol. 2025, 47(1), 41; https://doi.org/10.3390/cimb47010041 - 9 Jan 2025
Abstract
Polydeoxyribonucleotide (PDRN) has emerged as a potent bioactive compound with proven efficacy in wound healing, tissue regeneration, and anti-inflammatory applications and is predominantly derived from salmonid gonads. However, this study presents a groundbreaking advancement by successfully extracting and characterizing PDRN from microbial sources,
[...] Read more.
Polydeoxyribonucleotide (PDRN) has emerged as a potent bioactive compound with proven efficacy in wound healing, tissue regeneration, and anti-inflammatory applications and is predominantly derived from salmonid gonads. However, this study presents a groundbreaking advancement by successfully extracting and characterizing PDRN from microbial sources, specifically Lactobacillus rhamnosus, marking the first report to utilize microbial-, biome-, or Lactobacillus-derived PDRN (L-PDRN). The findings demonstrate the enhanced biological properties of L-PDRN over traditional salmon-derived PDRN across several assays. L-PDRN exhibited superior antioxidant activity, with significantly higher SOD-like and DPPH radical scavenging activities compared to PDRN, particularly at higher concentrations. In wound-healing assays, L-PDRN demonstrated superior efficacy in promoting cell migration and wound closure, even under inflammatory conditions induced by tumor necrosis factor (TNF-α). Additionally, L-PDRN demonstrated the potential for enhanced immunostimulatory effects under non-inflammatory conditions while maintaining anti-inflammatory properties under lipopolysaccharide (LPS) stimulation. Electrophoretic analysis revealed that L-PDRN consists of smaller DNA fragments (under 100 bp) compared to salmon-derived PDRN (200–800 bp), suggesting greater bioavailability and skin absorption. Mechanistic studies confirmed that L-PDRN activates the focal adhesion kinase (FAK) and protein kinase B (AKT) signaling pathway through the A2A receptor, similar to PDRN, while also engaging alternative pathways for p38 and ERK phosphorylation, highlighting its signaling versatility. This study underscores the potential of L-PDRN as a multifunctional and sustainable alternative to salmon-derived PDRN, offering enhanced bioactivity, scalability, and environmental benefits. The novel approach of utilizing microbial-derived PDRN opens new avenues for therapeutic applications in oxidative stress management, tissue regeneration, and immune modulation, paving the way for a paradigm shift in PDRN sourcing and functionality.
Full article
(This article belongs to the Special Issue The Role of Bioactives in Inflammation)
►▼
Show Figures
Figure 1
Open AccessArticle
A Theoretical Study on the Efficacy and Mechanism of Combined YAP-1 and PARP-1 Inhibitors in the Treatment of Glioblastoma Multiforme Using Peruvian Maca Lepidium meyenii
by
Albert Gabriel Turpo-Peqqueña, Sebastian Luna-Prado, Renato Javier Valencia-Arce, Fabio Leonardo Del-Carpio-Carrazco and Badhin Gómez
Curr. Issues Mol. Biol. 2025, 47(1), 40; https://doi.org/10.3390/cimb47010040 - 9 Jan 2025
Abstract
Glioblastoma multiforme (GBM) is one of the most aggressive and treatment-resistant forms of brain cancer. Current therapeutic strategies, including surgery, chemotherapy, and radiotherapy, often fail due to the tumor’s ability to develop resistance. The proteins YAP-1 (Yes-associated protein 1) and PARP-1 (Poly-(ADP-ribose)–polymerase-1) have
[...] Read more.
Glioblastoma multiforme (GBM) is one of the most aggressive and treatment-resistant forms of brain cancer. Current therapeutic strategies, including surgery, chemotherapy, and radiotherapy, often fail due to the tumor’s ability to develop resistance. The proteins YAP-1 (Yes-associated protein 1) and PARP-1 (Poly-(ADP-ribose)–polymerase-1) have been implicated in this resistance, playing crucial roles in cell proliferation and DNA repair mechanisms, respectively. This study explored the inhibitory potential of natural compounds from Lepidium meyenii (Peruvian Maca) on the YAP-1 and PARP-1 protein systems to develop novel therapeutic strategies for GBM. By molecular dynamics simulations, we identified N-(3-Methoxybenzyl)-(9Z,12Z,15Z)- octadecatrienamide (DK5) as the most promising natural inhibitor for PARP-1 and stearic acid (GK4) for YAP-1. Although synthetic inhibitors, such as Olaparib (ODK) for PARP-1 and Verteporfin (VER) for YAP-1, only VER was superior to the naturally occurring molecule and proved a promising alternative. In conclusion, natural compounds from Lepidium meyenii (Peruvian Maca) offer a potentially innovative approach to improve GBM treatment, complementing existing therapies with their inhibitory action on PARP-1 and YAP-1.
Full article
(This article belongs to the Section Molecular Pharmacology)
►▼
Show Figures
Figure 1
Open AccessReview
The Strong Inhibition of Pancreatic Lipase by Selected Indonesian Medicinal Plants as Anti-Obesity Agents
by
Min Rahminiwati, Dyah Iswantini, Trivadila, Rut Novalia Rahmawati Sianipar, Rani Melati Sukma, Susi Indariani and Anggia Murni
Curr. Issues Mol. Biol. 2025, 47(1), 39; https://doi.org/10.3390/cimb47010039 - 9 Jan 2025
Abstract
Obesity is characterized by the accumulation of excessive fat, potentially leading to degenerative diseases. Pancreatic lipase, an enzyme responsible for converting 50–70% of dietary fat into monoglycerides, free fatty acids, and various other smaller molecules, plays a crucial role in fat metabolism. Therefore,
[...] Read more.
Obesity is characterized by the accumulation of excessive fat, potentially leading to degenerative diseases. Pancreatic lipase, an enzyme responsible for converting 50–70% of dietary fat into monoglycerides, free fatty acids, and various other smaller molecules, plays a crucial role in fat metabolism. Therefore, this study aimed to review selected Indonesian medicinal plants with the potential to inhibit the activity of the pancreatic lipase enzyme. The results showed that kunci pepet (Kaempferiae angustifolia Rosc.), asam gelugur (Garcinia atroviridis), temulawak (Curcuma xanthorrhiza), jombang (Taraxacum officinale F. H. Wigg), pegagan (Centella asiatica), and pala (Myristica fragrans) had strong inhibitory effects, exceeding 50% for both in vitro and in vivo studies. Therefore, further studies are needed to explore the potential of these medicinal plants as anti-obesity treatments.
Full article
(This article belongs to the Special Issue New Insight: Enzymes as Targets for Drug Development, 2nd Edition)
►▼
Show Figures
Figure 1
Open AccessArticle
Methyl Canthin-6-one-2-carboxylate Inhibits the Activation of the NLRP3 Inflammasome in Synovial Macrophages by Upregulating Nrf2 Expression
by
Yuanyuan Chen, Zongying Zhang, Yuan Yao, Xiaorong Zhou, Yong Ling, Liming Mao and Zhifeng Gu
Curr. Issues Mol. Biol. 2025, 47(1), 38; https://doi.org/10.3390/cimb47010038 - 9 Jan 2025
Abstract
Rheumatoid arthritis (RA) is an autoimmune disorder that leads to severe cartilage deterioration and synovial impairment in the joints. Previous studies have indicated that the aberrant activation of the NLRP3 inflammasome in synovial macrophages plays a significant role in the pathogenesis of RA
[...] Read more.
Rheumatoid arthritis (RA) is an autoimmune disorder that leads to severe cartilage deterioration and synovial impairment in the joints. Previous studies have indicated that the aberrant activation of the NLRP3 inflammasome in synovial macrophages plays a significant role in the pathogenesis of RA and has been regarded as a therapeutic target for the disease. In this study, we synthesized a novel canthin-6-one alkaloid, namely methyl canthin-6-one-2-carboxylate (Cant), and assessed its effects on NLRP3 inflammasome activation in macrophages. Our data reveal that exposure to Cant significantly suppressed the transcription and secretion of multiple pro-inflammatory mediators, including IL-1β, IL-6, IL-18, TNF-α, NO, and COX2, in a dose-dependent manner. These alterations were associated with changes in the activation of various signaling pathways, including NF-kB, MAPK, and PI3K-AKT pathways. Notably, pretreatment with Cant significantly reduced LPS/ATP-induced activation of the NLRP3 inflammasome, as evidenced by the decline in the cleaved forms of IL-1β and caspase-1 in cell culture supernatants of BMDMs. Regarding the mechanisms, our data show that Cant could enhance the expression of Nrf2 in macrophages, which play an inhibitory role in ROS production. Collectively, our data demonstrate that Cant might suppress the activation of the NLRP3 inflammasome by upregulating the production of Nrf2, suggesting that Cant could serve as a candidate for the further development of anti-RA drugs.
Full article
(This article belongs to the Special Issue The Role of Bioactives in Inflammation)
►▼
Show Figures
Figure 1
Open AccessArticle
CD40 Ligand Potentiates Immunogenecity of Mycoplasma pneumoniae Subunit Vaccine Candidate in a Murine Model
by
Jinqi Shu, Gaojian Li, Jianhong Shu, Huapeng Feng and Yulong He
Curr. Issues Mol. Biol. 2025, 47(1), 37; https://doi.org/10.3390/cimb47010037 - 9 Jan 2025
Abstract
Mycoplasma hyopneumoniae (Mhp) infection severely affects the daily weight gain and feed-to-meat ratio of pigs, while secondary infections with other pathogens can further lead to increased mortality, causing significant economic losses to the pig industry. CD40L is a molecular adjuvant that enhances the
[...] Read more.
Mycoplasma hyopneumoniae (Mhp) infection severely affects the daily weight gain and feed-to-meat ratio of pigs, while secondary infections with other pathogens can further lead to increased mortality, causing significant economic losses to the pig industry. CD40L is a molecular adjuvant that enhances the cellular and humoral immune responses to vaccines. In this study, the CD40L peptide was fused to the C-terminus of the chimeric P97R1P46P42 protein by genetic engineering using the pFastBac Dual vector. The recombinant chimeric protein P97R1P46P42 and its fusion P97R1P46P42-CD40L were expressed in Sf9 cells and purified. Mice were immunized with P97R1P46P42 or its fusion protein. Seppic ISA 201 emulsified protein, conventional Mhp vaccine and PBS control groups were included. Immunogenecity was assessed by specific IgG antibody response, splenic lymphocyte proliferation, and cytokine IL-4 and IFN-γ levels. We found that CD40L fusion significantly enhanced specific antibody response, lymphocyte proliferation and IL-4 level in the immunized mouse sera as compared to the P97R1P46P42 or conventional vaccine group. This study provides clear evidence that CD40L potentiates the humoral and cellular immune responses to the Mhp chimeric protein P97R1P46P42 in the mouse model. This CD40L-fused chimeric protein could be a MPS subunit vaccine candidate to be tested for its efficacy in pigs in response to challenges with pathogenic Mycoplasma hyopneumoniae strain(s).
Full article
(This article belongs to the Special Issue Recombinant Proteins for Molecular Biology Research: Technologies and Applications)
►▼
Show Figures
Figure 1
Open AccessArticle
Exploring the Anticancer Potential of MonoHER (7-Mono-O-(β-Hydroxyethyl)-Rutoside): Mitochondrial-Dependent Apoptosis in HepG2 Cells
by
Chujie Li, Yue Wang, Jian Liang, Guido R. M. M. Haenen, Yonger Chen, Zhengwen Li, Ming Zhang and Ludwig J. Dubois
Curr. Issues Mol. Biol. 2025, 47(1), 36; https://doi.org/10.3390/cimb47010036 - 9 Jan 2025
Abstract
Background/Aim: Flavonoids are a group of polyphenols, abundantly present in our diet. Although, based on their chemoprotective effects, intake of flavonoids is associated with a high anticancer potential as evidenced in in vitro and in vivo models, the molecular mechanism is still elusive.
[...] Read more.
Background/Aim: Flavonoids are a group of polyphenols, abundantly present in our diet. Although, based on their chemoprotective effects, intake of flavonoids is associated with a high anticancer potential as evidenced in in vitro and in vivo models, the molecular mechanism is still elusive. This study explores the antiproliferative and cytotoxic effects of the semi-synthetic flavonoid MonoHER (7-mono-O-(β-hydroxyethyl)-rutoside) in vitro on cancer cells. Materials and Methods: HepG2 liver, MCF7 breast, and H1299 lung cancer cells were grown under ambient conditions with or without MonoHER exposure. CCK8 assay was used to assess cell viability. Apoptosis, JC-1, and mitochondrial mass were determined using flow cytometry and confocal analysis. The effects of monoHER on apoptosis proteins were detected by confocal microscopy analysis and Western blot. Results: It was found that MonoHER can reduce HepG2 cells’ and MCF7 cells’ viability, but not H1299 cells’, and induced apoptosis only in HepG2 cells. MonoHER has the potential to enhance the expression of caspase-9 and caspase-3, to damage mitochondria, and to provoke the release of cytochrome C from the mitochondria. Conclusion: MonoHER can inhibit cell growth and induce apoptosis especially in HepG2 human liver cancer cells by triggering the mitochondrial signal transduction pathway, leading to the release of cytochrome C in the cytoplasm and the subsequent activation of caspase-9 and caspase-3. Future research should further explore MonoHER’s mechanism of action, efficacy, and potential for clinical translation.
Full article
(This article belongs to the Special Issue The Role of Natural Compounds in Cancer Therapy)
►▼
Show Figures
Figure 1
Open AccessArticle
GFAPβ and GFAPδ Isoforms Expression in Mesenchymal Stem Cells, MSCs Differentiated Towards Schwann-like, and Olfactory Ensheathing Cells
by
Nidia Jannette Carrillo González, Gabriela Stefania Reyes Gutierrez, Tania Campos-Ordoñez, Rubén D. Castro-Torres, Carlos Beas Zárate and Graciela Gudiño-Cabrera
Curr. Issues Mol. Biol. 2025, 47(1), 35; https://doi.org/10.3390/cimb47010035 - 9 Jan 2025
Abstract
Olfactory ensheathing cells (OECs) and mesenchymal stem cells (MSCs) differentiated towards Schwann-like have plasticity properties. These cells express the Glial fibrillary acidic protein (GFAP), a type of cytoskeletal protein that significantly regulates many cellular functions, including those that promote cellular plasticity needed for
[...] Read more.
Olfactory ensheathing cells (OECs) and mesenchymal stem cells (MSCs) differentiated towards Schwann-like have plasticity properties. These cells express the Glial fibrillary acidic protein (GFAP), a type of cytoskeletal protein that significantly regulates many cellular functions, including those that promote cellular plasticity needed for regeneration. However, the expression of GFAP isoforms (α, β, and δ) in these cells has not been characterized. We evaluated GFAP isoforms (α, β, and δ) expression by Polymerase Chain Reaction (PCR) assay in three conditions: (1) OECs, (2) cells exposed to OECs-conditioned medium and differentiated to Schwann-like cells (dBM-MSCs), and (3) MSC cell culture from rat bone marrow undifferentiated (uBM-MSCs). First, the characterization phenotyping was verified by morphology and immunocytochemistry, using p75, CD90, and GFAP antibodies. Then, we found the expression of GFAP isoforms (α, β, and δ) in the three conditions; the expression of the GFAPα (10.95%AUC) and GFAPβ (9.17%AUC) isoforms was predominantly in OECs, followed by dBM-MSCs (α: 3.99%AUC, β: 5.66%AUC) and uBM-MSCs (α: 2.47%AUC, β: 2.97%AUC). GFAPδ isoform has a similar expression in the three groups (OEC: 9.21%AUC, dBM-MSCs: 11.10%AUC, uBM-MSCs: 9.21%AUC). These findings suggest that expression of different GFAPδ and GFAPβ isoforms may regulate cellular plasticity properties, potentially contributing to tissue remodeling processes by OECs, dBM-MSCs, and uBM-MSCs.
Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
►▼
Show Figures
Graphical abstract
Open AccessReview
The Development of Methods of BLOTCHIP®-MS for Peptidome: Small Samples in Tuberous Sclerosis
by
Kunio Yui, George Imataka, Kotaro Yuge, Hitomi Sasaki, Tadashi Shiohama, Kyoichi Asada and Hidehisa Tachiki
Curr. Issues Mol. Biol. 2025, 47(1), 34; https://doi.org/10.3390/cimb47010034 - 7 Jan 2025
Abstract
Mutations in TSC1 or TSC2 in axons induce tuberous sclerosis complex. Neurological manifestations mainly include epilepsy and autism spectrum disorder (ASD). ASD is the presenting symptom (25–50% of patients). ASD was observed at significantly higher frequencies in participants with TSC2 than those with
[...] Read more.
Mutations in TSC1 or TSC2 in axons induce tuberous sclerosis complex. Neurological manifestations mainly include epilepsy and autism spectrum disorder (ASD). ASD is the presenting symptom (25–50% of patients). ASD was observed at significantly higher frequencies in participants with TSC2 than those with TSC1 mutations. The occurrence of TSC2 mutations is about 50% larger than TSC1. Therefore, ASD may develop due to TSC2 deficiency. TSC2 regulates microRNA biogenesis and Microprocessor activity via GSK3β. Of reference, everolimus has the best treatment target because of the higher potency of interactions with mTORC2 rather than rapamycin. Mutations in the TSC1 and TSC2 genes result in the constitutive hyperactivation of the mammalian target of the rapamycin (mTOR) pathway, contributing to the growth of benign tumors or hamartomas in various organs. TSC2 mutations were associated with a more severe phenotypic spectrum than TSC1 mutations because of the inhibition of the mTOR cascade. There are few studies on the peptide analysis of this disorder in relation to everolimus. Only one study reported that, in ten plasma samples, pre-melanosome protein (PMEL) and S-adenosylmethionine (SAM) were significantly changed as diagnostic prognostic effects. Our study on peptide analysis in Protosera Inc (Osaka, Japan) revealed that three peptides that were related to inflammation in two patients with tuberous sclerosis, who showed a 30% decrease in ASD symptoms following everolimus treatment. TSC2 mutations were associated with a more severe phenotypic spectrum due to the inhibition of the mTOR cascade. PMEL and SAM were significantly changed as diagnostic effects.
Full article
(This article belongs to the Topic Autism: Molecular Bases, Diagnosis and Therapies, 2nd Volume)
►▼
Show Figures
Figure 1
Open AccessArticle
Antiedemic Effect of the Myosin Light Chain Kinase Inhibitor PIK7 in the Rat Model of Myocardial Ischemia Reperfusion Injury
by
Dmitry L. Sonin, Mikhail S. Medved, Asker Y. Khapchaev, Maria V. Sidorova, Marina E. Palkeeva, Olga A. Kazakova, Garry V. Papayan, Daniil A. Mochalov, Sarkis M. Minasyan, Ilya E. Anufriev, Daria V. Mukhametdinova, Natalia M. Paramonova, Ksenia M. Balabanova, Anastasia S. Lopatina, Ilia V. Aleksandrov, Natalya Yu. Semenova, Anna A. Kordyukova, Kirill V. Zaichenko, Vladimir P. Shirinsky and Michael M. Galagudza
Curr. Issues Mol. Biol. 2025, 47(1), 33; https://doi.org/10.3390/cimb47010033 - 6 Jan 2025
Abstract
Myocardial ischemia-reperfusion injury increases myocardial microvascular permeability, leading to enhanced microvascular filtration and interstitial fluid accumulation that is associated with greater microvascular obstruction and inadequate myocardial perfusion. A burst of reactive oxygen species and inflammatory mediators during reperfusion causes myosin light chain kinase
[...] Read more.
Myocardial ischemia-reperfusion injury increases myocardial microvascular permeability, leading to enhanced microvascular filtration and interstitial fluid accumulation that is associated with greater microvascular obstruction and inadequate myocardial perfusion. A burst of reactive oxygen species and inflammatory mediators during reperfusion causes myosin light chain kinase (MLCK)-dependent endothelial hyperpermeability, which is considered a preventable cause of reperfusion injury. In the present study, a single intravenous injection of MLCK peptide inhibitor PIK7 (2.5 mg/kg or 40 mg/kg) was found to suppress the vascular hyperpermeability caused by ischemia/reperfusion injury in an in vivo rat model. The antiedemic effect of PIK7 is transient and ceases within 90 min of reperfusion. The early no-reflow detected for the first time after 30 min ischemia in this model of myocardial infarction reduces the area accessible for PIK7. Electron microscopy has shown membrane-bound blebs of endotheliocytes, which partially or completely obturate the capillary lumen, and few capillaries with signs of intercellular gap formation in samples obtained from the center of the early no-reflow zone in control and PIK7-injected rats. Co-injection of PIK7 with NO donor sodium nitroprusside (SNP) increases blood flow in the zone of early no-reflow, while reducing the increased vascular permeability caused by SNP.
Full article
(This article belongs to the Section Molecular Medicine)
►▼
Show Figures
Figure 1
Open AccessArticle
Prognostic Value of PSMB5 and Correlations with LC3II and Reactive Oxygen Species Levels in the Bone Marrow Mononuclear Cells of Bortezomib-Resistant Multiple Myeloma Patients
by
Eva Plakoula, Georgios Kalampounias, Spyridon Alexis, Evgenia Verigou, Alexandra Kourakli, Kalliopi Zafeiropoulou and Argiris Symeonidis
Curr. Issues Mol. Biol. 2025, 47(1), 32; https://doi.org/10.3390/cimb47010032 - 6 Jan 2025
Abstract
Proteasome inhibitors (PIs) constitute the most common type of induction treatment for multiple myeloma. Interactions between the proteasome, autophagy, and reactive oxygen species (ROS) have been shown in the past, thus emphasizing the need for a better understanding of the underlying pathophysiology. For
[...] Read more.
Proteasome inhibitors (PIs) constitute the most common type of induction treatment for multiple myeloma. Interactions between the proteasome, autophagy, and reactive oxygen species (ROS) have been shown in the past, thus emphasizing the need for a better understanding of the underlying pathophysiology. For this study, bone marrow mononuclear cells from 110 myeloma patients were collected at different disease stages. PSMB5 and LC3I/II protein levels were determined using Western blot, proteasome proteolytic activity (PPA) with spectrofluorometry, and ROS with flow cytometry. PSMB5 accumulation was found to diminish after PI treatment (p-value = 0.014), and the same pattern was observed in PPA (p-value < 0.001). Conversely, LC3II protein levels were elevated at both remission and relapse compared to baseline levels (p-value = 0.041). Patients with a baseline PSMB5 accumulation lower than 1.06 units had longer disease-free survival compared to those with values above 1.06 units (12.0 ± 6.7 vs. 36 ± 12.1 months; p-value < 0.001). Median ROS levels in plasma cells were significantly higher at relapse compared to both baseline and remission levels (p-value < 0.001), implying poor prognosis. Overall, post-treatment PSMB5 reduction could indicate a shift from proteasomal to autophagic degradation as a main proteostatic mechanism, thus explaining resistance. The elevated oxidative stress in PI-treated patients could possibly serve as an additional compensatory mechanism.
Full article
(This article belongs to the Special Issue Molecular Insights and Therapeutic Advances in Hematological Disorders)
►▼
Show Figures
Figure 1
Open AccessArticle
The Effect of Autologous Dendritic Cell Immunotherapy on Kidney Function and Endothelial Dysfunction of Patients with Diabetic Kidney Disease (DKD): An Open Label Clinical Trial
by
Martina Lily Yana, Enda Cindylosa Sitepu, Jonny, Linda Chiuman, I Nyoman Ehrich Lister and Terawan Agus Putranto
Curr. Issues Mol. Biol. 2025, 47(1), 31; https://doi.org/10.3390/cimb47010031 - 6 Jan 2025
Abstract
This study aimed to evaluate the effects of autologous dendritic cell (DC) immunotherapy on clinical outcomes (glomerular filtration rate/GFR and urine creatinine albumin ratio/UACR) and endothelial dysfunction (ICAM, VCAM, VEGF) in patients with diabetic kidney disease (DKD). Endothelial dysfunction induced by inflammation is
[...] Read more.
This study aimed to evaluate the effects of autologous dendritic cell (DC) immunotherapy on clinical outcomes (glomerular filtration rate/GFR and urine creatinine albumin ratio/UACR) and endothelial dysfunction (ICAM, VCAM, VEGF) in patients with diabetic kidney disease (DKD). Endothelial dysfunction induced by inflammation is one of the key factors in the pathogenesis of DKD. In this one-group pretest–posttest quasi-experimental study, 69 subjects with DKD were administered a single dose of autologous DC immunotherapy ex vivo. UACR was measured at baseline and at weeks 1, 2, 3, and 4, while ICAM, VCAM, VEGF, and GFR were measured at baseline and at week 4 post-immunotherapy. The results showed a significant reduction in median UACR from 250 (IQR 71–668) mg/g at baseline to 164 (IQR 49–576) mg/g at week 4 (p < 0.05). GFR did not show any significant changes after immunotherapy. HbA1c (B = −33.270, p = 0.021) and baseline UACR (B = −0.185, p < 0.001) were identified as significant predictors of UACR change. Although there were no significant changes in ICAM, VCAM, and VEGF, subgroup analysis revealed a decrease in VCAM in macroalbuminuria patients and an increase in those with good glycemic control, suggesting differing endothelial responses. In conclusion, autologous DC immunotherapy effectively reduced UACR in DKD patients, and significant VCAM changes were found in macroalbuminuria and good glycemic control subjects. Further research is needed to understand the mechanisms behind UACR reduction and the long-term impact of this therapy.
Full article
(This article belongs to the Special Issue Diabetes and Its Complications: Unraveling the Molecular Landscapes of a Metabolic Conundrum)
►▼
Show Figures
Figure 1
Open AccessReview
Phytochemicals in Breast Cancer Prevention and Treatment: A Comprehensive Review
by
Adil Farooq Wali, Jayachithra Ramakrishna Pillai, Sirajunisa Talath, Pooja Shivappa, Sathvik Belagodu Sridhar, Mohamed El-Tanani, Imran Rashid Rangraze, Omnia Ibrahim Mohamed and Nowar Nizar Al Ani
Curr. Issues Mol. Biol. 2025, 47(1), 30; https://doi.org/10.3390/cimb47010030 - 6 Jan 2025
Abstract
Extensive investigation has been conducted on plant-based resources for their pharmacological usefulness, including various cancer types. The scope of this review is wider than several studies with a particular focus on breast cancer, which is an international health concern while studying sources of
[...] Read more.
Extensive investigation has been conducted on plant-based resources for their pharmacological usefulness, including various cancer types. The scope of this review is wider than several studies with a particular focus on breast cancer, which is an international health concern while studying sources of flavonoids, carotenoids, polyphenols, saponins, phenolic compounds, terpenoids, and glycosides apart from focusing on nursing. Important findings from prior studies are synthesized to explore these compounds’ sources, mechanisms of action, complementary and synergistic effects, and associated side effects. It was reviewed that the exposure to certain doses of catechins, piperlongumine, lycopene, isoflavones and cucurbitacinfor a sufficient period can provide profound anticancer benefits through biological events such as cell cycle arrest, cells undergoing apoptosis and disruption of signaling pathways including, but not limited to JAK-STAT3, HER2-integrin, and MAPK. Besides, the study also covers the potential adverse effects of these phytochemicals. Regarding mechanisms, the widest attention is paid to Complementary and synergistic strategies are discussed which indicate that it would be realistic to alter the dosage and delivery systems of liposomes, nanoparticles, nanoemulsions, and films to enhance efficacy. Future research directions include refining these delivery approaches, further elucidating molecular mechanisms, and conducting clinical trials to validate findings. These efforts could significantly advance the role of phytocompounds in breast cancer management.
Full article
(This article belongs to the Special Issue Phytochemicals and Cancer, 2nd Edition)
►▼
Show Figures
Figure 1
Open AccessArticle
Identification of Potential Selective PAK4 Inhibitors Through Shape and Protein Conformation Ensemble Screening and Electrostatic-Surface-Matching Optimization
by
Xiaoxuan Zhang, Meile Zhang, Yihao Li and Ping Deng
Curr. Issues Mol. Biol. 2025, 47(1), 29; https://doi.org/10.3390/cimb47010029 - 6 Jan 2025
Abstract
P21-activated kinase 4 (PAK4) plays a crucial role in the proliferation and metastasis of various cancers. However, developing selective PAK4 inhibitors remains challenging due to the high homology within the PAK family. Therefore, developing highly selective PAK4 inhibitors is critical to overcoming the
[...] Read more.
P21-activated kinase 4 (PAK4) plays a crucial role in the proliferation and metastasis of various cancers. However, developing selective PAK4 inhibitors remains challenging due to the high homology within the PAK family. Therefore, developing highly selective PAK4 inhibitors is critical to overcoming the limitations of existing inhibitors. We analyzed the structural differences in the binding pockets of PAK1 and PAK4 by combining cross-docking and molecular dynamics simulations to identify key binding regions and unique structural features of PAK4. We then performed screening using shape and protein conformation ensembles, followed by a re-evaluation of the docking results with deep-learning-driven GNINA to identify the candidate molecule, STOCK7S-56165. Based on this, we applied a fragment-replacement strategy under electrostatic-surface-matching conditions to obtain Compd 26. This optimization significantly improved electrostatic interactions and reduced binding energy, highlighting its potential for selectivity. Our findings provide a novel approach for developing selective PAK4 inhibitors and lay the theoretical foundation for future anticancer drug design.
Full article
(This article belongs to the Special Issue New Insight: Enzymes as Targets for Drug Development, 2nd Edition)
►▼
Show Figures
Figure 1
Open AccessReview
Molecular Findings Before Vision Loss in the Streptozotocin-Induced Rat Model of Diabetic Retinopathy
by
Mădălina Moldovan, Roxana-Denisa Capraș, Raluca Paşcalău and Gabriela Adriana Filip
Curr. Issues Mol. Biol. 2025, 47(1), 28; https://doi.org/10.3390/cimb47010028 - 4 Jan 2025
Abstract
The streptozotocin-induced rat model of diabetic retinopathy presents similarities to the disease observed in humans. After four weeks following the induction of diabetes, the rats experience vision impairment. During this crucial four-week period, significant changes occur, with vascular damage standing out as a
[...] Read more.
The streptozotocin-induced rat model of diabetic retinopathy presents similarities to the disease observed in humans. After four weeks following the induction of diabetes, the rats experience vision impairment. During this crucial four-week period, significant changes occur, with vascular damage standing out as a clinically significant factor, alongside neovascularization. While redox imbalance, activation of microglia, secretion of pro-inflammatory cytokines, and neuronal cell death are also observed, the latter remains an emerging hypothesis requiring further exploration. This review is a comprehensive and up-to-date chronological depiction of the progression of diabetic retinopathy within the initial four weeks of hyperglycemia, which precede the onset of vision loss. The data are structured in weekly changes. In the first week, oxidative stress triggers the activation of retinal microglia, which produces inflammation, leading to altered neurotransmission. The second week is characterized by leukostasis, which promotes ischemia, while neural degeneration begins and is accompanied by a simultaneous increase in vessel permeability. The progression of redox and inflammatory imbalances characterized the third week. Finally, in the fourth week, significant developments occur as vessels dilate and become tortuous, neovascularization develops, and retinal thickness diminishes, ultimately leading to vision loss. Through this clearly structured outline, this review aims to delineate a framework for the progression of streptozotocin-induced diabetic retinopathy.
Full article
(This article belongs to the Special Issue Diabetes and Its Complications: Unraveling the Molecular Landscapes of a Metabolic Conundrum)
►▼
Show Figures
Figure 1
Open AccessArticle
Serum hsa-miR-22-3p, hsa-miR-885-5p, Lipase-to-Amylase Ratio, C-Reactive Protein, CA19-9, and Neutrophil-to-Lymphocyte Ratio as Prognostic Factors in Advanced Pancreatic Ductal Adenocarcinoma
by
Jakub Wnuk, Dorota Hudy, Joanna Katarzyna Strzelczyk, Łukasz Michalecki, Kamil Dybek and Iwona Gisterek-Grocholska
Curr. Issues Mol. Biol. 2025, 47(1), 27; https://doi.org/10.3390/cimb47010027 - 3 Jan 2025
Abstract
Pancreatic cancer (PC) is the seventh most common cause of cancer-related death worldwide. The low survival rate may be due to late diagnosis and asymptomatic early-stage disease. Most patients are diagnosed at an advanced stage of the disease. The search for novel prognostic
[...] Read more.
Pancreatic cancer (PC) is the seventh most common cause of cancer-related death worldwide. The low survival rate may be due to late diagnosis and asymptomatic early-stage disease. Most patients are diagnosed at an advanced stage of the disease. The search for novel prognostic factors is still needed. Two miRNAs, miR-22-3p and miR-885-5p, which show increased expression in PC, were selected for this study. The aim of this study was to evaluate the utility of these miRNAs in the prognosis of PC. Other prognostic factors such as lipase-to-amylase ratio (LAR), neutrophil-to-lymphocyte ratio (NLR), and carbohydrate antigen 19-9 (CA19-9) were also evaluated in this study. This study was conducted in 50 patients previously diagnosed with pancreatic ductal adenocarcinoma in clinical stage (CS) III and IV. All patients underwent a complete medical history, physical examination, and routine laboratory tests including a complete blood count, C-reactive protein (CRP), CA19-9, lipase, and amylase. Two additional blood samples were taken from each patient to separate plasma and serum. Isolation of miRNA was performed using TRI reagent with cel-miR-39-3p as a spike-in control. Reverse transcription of miRNA was performed using a TaqMan Advanced miRNA cDNA Synthesis Kit. The relative expression levels of miR-22-3p and miR-885-5p were measured using RT-qPCR. Serum hsa-miR-22-3p was detected in 22 cases (44%), while hsa-miR-885-5p was detected in 33 cases (66%). There were no statistically significant differences in serum or plasma miRNA expression levels between patient groups based on clinical stage, gender, or BMI. There were no statistically significant differences in LAR between patients with different CS. For NLR, CRP and CA19-9 thresholds were determined using ROC analysis (6.63, 24.7 mg/L and 4691 U/mL, respectively). Cox’s F test for overall survival showed statistically significant differences between groups (p = 0.002 for NLR, p = 0.007 for CRP and p = 0.007 for CA19-9). Utility as prognostic biomarkers was confirmed in univariate and multivariate analysis for CA19-9, CRP, and NLR. The selected miRNAs and LAR were not confirmed as reliable prognostic markers in PC.
Full article
(This article belongs to the Special Issue The Significance of Transcription Factors, miRNAs, and lncRNAs in Anticancer Drug Development)
►▼
Show Figures
Figure 1
Open AccessCase Report
1q21.1 Duplication Syndrome and Anorectal Malformations: A Literature Review and a New Case
by
Maria Minelli, Chiara Palka Bayard de Volo, Melissa Alfonsi, Serena Capanna, Elisena Morizio, Maria Enrica Miscia, Gabriele Lisi, Liborio Stuppia and Valentina Gatta
Curr. Issues Mol. Biol. 2025, 47(1), 26; https://doi.org/10.3390/cimb47010026 - 3 Jan 2025
Abstract
Background: Anorectal malformations (ARMs) are a common pediatric surgical problem with an incidence of 1:1500 to 1:5000 live births. The phenotypical spectrum extends from anal stenosis to imperforate anus with or without anal fistula to persistent cloaca. They can manifest as either non-syndromic
[...] Read more.
Background: Anorectal malformations (ARMs) are a common pediatric surgical problem with an incidence of 1:1500 to 1:5000 live births. The phenotypical spectrum extends from anal stenosis to imperforate anus with or without anal fistula to persistent cloaca. They can manifest as either non-syndromic or syndromic conditions. Various environmental and genetic risk factors have been elucidated. The widespread use of genetic screening tests for the investigation of developmental disorders increased the recognition of copy number variants (CNVs) of the 1q21.1 region. Duplications have also been associated with a multitude of congenital anomalies, such as heart disease, short stature, scoliosis, urogenital, and ARMs, and they have also been found in healthy individuals. The aim of this manuscript is to contribute to the definition of the phenotype associated with 1q21.1 duplications. Case presentation: The present case describes a male, referred to us for an ARM, in whom array—comparative genomic hybridization (array-CGH) identified 1q21.1 duplication inherited from his healthy mother. No other genetic test was performed on the patient. Conclusions: We propose considering genetic evaluation and analysis in patients with only one congenital malformation in order to eventually make an early diagnosis and a better quality of treatments.
Full article
(This article belongs to the Special Issue Genomic Analysis of Common Disease)
►▼
Show Figures
Figure 1
Journal Menu
► ▼ Journal MenuJournal Browser
► ▼ Journal Browser-
arrow_forward_ios
Forthcoming issue
arrow_forward_ios Current issue - Volumes not published by MDPI
- Vol. 42 (2021)
- Vol. 41 (2021)
- Vol. 40 (2021)
- Vol. 39 (2020)
- Vol. 38 (2020)
- Vol. 37 (2020)
- Vol. 36 (2020)
- Vol. 35 (2020)
- Vol. 34 (2019)
- Vol. 33 (2019)
- Vol. 32 (2019)
- Vol. 31 (2019)
- Vol. 30 (2019)
- Vol. 29 (2018)
- Vol. 28 (2018)
- Vol. 27 (2018)
- Vol. 26 (2018)
- Vol. 25 (2018)
- Vol. 24 (2017)
- Vol. 23 (2017)
- Vol. 22 (2017)
- Vol. 21 (2017)
- Vol. 20 (2016)
- Vol. 19 (2016)
- Vol. 18 (2016)
- Vol. 17 (2015)
- Vol. 16 (2014)
- Vol. 15 (2013)
- Vol. 14 (2012)
- Vol. 13 (2011)
- Vol. 12 (2010)
- Vol. 11 (2009)
- Vol. 10 (2008)
- Vol. 9 (2007)
- Vol. 8 (2006)
- Vol. 7 (2005)
- Vol. 6 (2004)
- Vol. 5 (2003)
- Vol. 4 (2002)
- Vol. 3 (2001)
- Vol. 2 (2000)
- Vol. 1 (1999)
Highly Accessed Articles
Latest Books
E-Mail Alert
News
7 January 2025
MDPI INSIGHTS: The CEO's Letter #19 - Reflecting on 2024, Society Journals, OA Germany
MDPI INSIGHTS: The CEO's Letter #19 - Reflecting on 2024, Society Journals, OA Germany
2 January 2025
Meet Us at the 58th European Human Genetics Conference (ESHG 2025), 24–27 May 2025, Milan, Italy
Meet Us at the 58th European Human Genetics Conference (ESHG 2025), 24–27 May 2025, Milan, Italy
Topics
Topic in
BioChem, Biomolecules, CIMB, Molecules, Pharmaceutics, Sci. Pharm.
Design, Synthesis and Biological Evaluation of Novel Small Molecules as Multi-target Enzyme Inhibitors
Topic Editors: Davide Moi, Daniele Passarella, Andrea CitarellaDeadline: 31 January 2025
Topic in
CIMB, Molecules, Pharmaceuticals, Pharmaceutics, Sci. Pharm.
Challenges and Opportunities in Drug Delivery Research
Topic Editors: Lenuta Profire, Ioana Mirela VasincuDeadline: 31 March 2025
Topic in
Biomedicines, Brain Sciences, CIMB, Diagnostics, IJMS, IJTM
Autism: Molecular Bases, Diagnosis and Therapies, 2nd Volume
Topic Editors: Lello Zolla, Kunio YuiDeadline: 31 May 2025
Topic in
Biomolecules, CIMB, Sci. Pharm., Cancers, Current Oncology, Cells
The Role of Extracellular Vesicles as Modulators of the Tumor Microenvironment
Topic Editors: Nils Ludwig, Miroslaw J SzczepanskiDeadline: 30 June 2025
Conferences
Special Issues
Special Issue in
CIMB
Phytochemicals in Cancer Chemoprevention and Treatment
Guest Editors: Wojciech Trybus, Ewa Trybus, Aneta Wȩgierek-CiukDeadline: 15 January 2025
Special Issue in
CIMB
Molecular Breeding and Genetics Research in Plants, 2nd Edition
Guest Editor: Shimeles TilahunDeadline: 20 January 2025
Special Issue in
CIMB
Radiation-Induced Cellular and Molecular Responses
Guest Editor: Carlo AprileDeadline: 20 January 2025
Special Issue in
CIMB
Advances and Challenges in Organ Decellularization and Recellularization
Guest Editor: Aylin AcunDeadline: 30 January 2025
Topical Collections
Topical Collection in
CIMB
Feature Papers in Current Issues in Molecular BiologyCollection Editor: Madhav Bhatia
Topical Collection in
CIMB
Molecular Mechanisms in Human Diseases
Collection Editor: Roberto Campagna
Topical Collection in
CIMB
Feature Papers Collection in Molecular Microbiology
Collection Editor: Bruce Seal