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Tumor Immune Microenvironment and Checkpoint Inhibition in Clear Cell Ovarian Carcinoma: Bridging Tumor Biology and Clinical Application in Immunotherapy
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The Central Nervous System Modulatory Activities of N-Acetylcysteine: A Synthesis of Two Decades of Evidence
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JUNB and JUND in Urological Cancers: A Literature Review
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Physical Activity and Metabolic Disorders—What Does Gut Microbiota Have to Do with It?
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The Role of miRNAs and Extracellular Vesicles in Adaptation After Resistance Exercise: A Review
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 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)
Latest Articles
The Tumor-Suppressive Role of SAT2 in Pancreatic Cancer: Involvement in PI3K/Akt-MAPK Pathways and Immune Modulation
Curr. Issues Mol. Biol. 2025, 47(10), 872; https://doi.org/10.3390/cimb47100872 - 21 Oct 2025
Abstract
Spermidine/spermine N1-Acetyltransferase 2 (SAT2), belonging to the spermidine/spermine N1-Acetyltransferase family, has been increasingly recognized for its potential effects on tumor occurrence and development. Nonetheless, little is known about its biological function and clinical value for pancreatic cancer (PC). The present work focused on
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Spermidine/spermine N1-Acetyltransferase 2 (SAT2), belonging to the spermidine/spermine N1-Acetyltransferase family, has been increasingly recognized for its potential effects on tumor occurrence and development. Nonetheless, little is known about its biological function and clinical value for pancreatic cancer (PC). The present work focused on investigating its expression pattern, prognostic value, molecular mechanisms, and immune relevance in PC. SAT2 expression within PC samples and its prognostic significance were analyzed by retrieving the relevant data from the TCGA, CPTAC, and HPA databases. The biological function of SAT2 was investigated through GO and KEGG enrichment analyses. The association of SAT2 with immune cell infiltration in tumors was assessed by CIBERSORT. Additionally, in vitro experiments were performed to examine how SAT2 expression affected the PC cell proliferation, invasion, and migration abilities. An in vivo xenograft tumor model was employed for investigating how SAT2 expression affected the PC cell-derived tumor growth. The expression of SAT2 within the PC tissue exhibited a significant decrease in comparison with a non-carcinoma sample. Such observation was validated within PC cells. In addition, SAT2 expression showed a close relation to both tumor growth (T stage) and prognosis. SAT2 primarily participates in pathways, including the PI3K/Akt and MAPK pathways. Furthermore, we demonstrated a significant association between SAT2 expression and immune cell infiltration into tumors. The in vitro experiments confirmed that elevated SAT2 expression significantly suppressed PC cell viability, invasion, and migration through modulating the PI3K/Akt and MAPK pathways. The in vivo experimental results suggested the role of SAT2 overexpression in inhibiting xenograft tumor growth. Our investigation confirms the role of SAT2 in PC development through involvement in the PI3K/Akt and MAPK pathways. The correlation between SAT2 expression levels, immune infiltration, and checkpoint regulation provides valuable insights for immunotherapy strategies targeting PC.
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(This article belongs to the Section Molecular Medicine)
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Study on Autophagy Death of Alpha TC1 Clone 6 (αTC1-6) Cells Induced by Trametenolic Acid Through PI3K/AKT Pathway
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Wangyang Ye, Shangling Pan, Hongqi Zhang, Xiaolan Zhang and Junzhi Wang
Curr. Issues Mol. Biol. 2025, 47(10), 871; https://doi.org/10.3390/cimb47100871 - 21 Oct 2025
Abstract
Glucagonoma, a rare neuroendocrine tumor, lacks targeted treatment drugs. Excessive secretion of glucagon is the main cause of its clinical syndrome. To explore targeted therapeutic drugs that can inhibit glucagon secretion and tumor proliferation, we investigated the effect of Trametenolic Acid (TA) on
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Glucagonoma, a rare neuroendocrine tumor, lacks targeted treatment drugs. Excessive secretion of glucagon is the main cause of its clinical syndrome. To explore targeted therapeutic drugs that can inhibit glucagon secretion and tumor proliferation, we investigated the effect of Trametenolic Acid (TA) on mouse pancreatic alpha TC1 clone 6 (αTC1-6) cells and its regulatory role in the PI3K/AKT signaling pathway. Cell viability of αTC1-6 cells was assessed via the MTT assay. Glucagon content in cell culture supernatants was measured using an Enzyme-Linked Immunosorbent Assay (ELISA). Autophagic vacuoles were visualized through Monodansylcadaverine (MDC) staining. The expression of autophagy-related proteins including Atg7, LC3 Ⅱ and PI3K/AKT signaling pathway-related proteins mTOR and FoxO1 were determined by Western blot. The results showed that the proliferation of αTC1-6 cells was significantly inhibited by TA in a dose- and time-dependent manner, and the IC50 was 140.71, 26.77 and 1.99 μM after treatment of 12, 24, and 48 h, respectively. The secretion of glucagon was significantly inhibited by TA. The MDC staining results showed that the fluorescent labeled autophagic vesicles in the TA group were increased. The Western blot results showed that the expression of Atg7 and LC3 Ⅱ was promoted by TA in a dose-dependent manner, the phosphorylation of PI3K, AKT, mTOR and FoxO1 was significantly inhibited, and the expression of FoxO1 protein was increased. These results demonstrated that TA can inhibit glucagon secretion, induce autophagy, and suppress cell proliferation in αTC1-6 cells. The mechanism may be associated with the PI3K/AKT signaling pathway.
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(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Open AccessArticle
Ethacridine Targets Bacterial Biofilms in Diabetic Foot Ulcers: A Multi-Target Mechanism Revealed by Network Pharmacology, Molecular Docking, Molecular Dynamics Simulation, and Clinical RT-qPCR Validation
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Tianbo Li, Yuming Zhuang, Jiangning Wang and Lei Gao
Curr. Issues Mol. Biol. 2025, 47(10), 870; https://doi.org/10.3390/cimb47100870 - 21 Oct 2025
Abstract
Objective: This study aimed to systematically investigate the potential antibacterial mechanisms of ethacridine in the treatment of diabetic foot ulcers (DFUs) by integrating network pharmacology, molecular docking, and molecular dynamics simulation approaches. Methods: The potential targets of ethacridine were predicted using the SwissTargetPrediction
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Objective: This study aimed to systematically investigate the potential antibacterial mechanisms of ethacridine in the treatment of diabetic foot ulcers (DFUs) by integrating network pharmacology, molecular docking, and molecular dynamics simulation approaches. Methods: The potential targets of ethacridine were predicted using the SwissTargetPrediction () and PharmMapper databases and subsequently converted to gene symbols via the UniProt database. DFU-related and antibacterial-related targets were retrieved from the GeneCards and OMIM databases. The overlapping targets among ethacridine, DFU, and antibacterial-related genes were identified as candidate therapeutic targets. A “drug–disease–target” network was constructed using Cytoscape, while protein–protein interaction (PPI) networks were built through the STRING database. GO and KEGG enrichment analyses were performed using R software. Molecular docking was conducted to evaluate the binding affinities between core compounds and hub targets. Furthermore, molecular dynamics (MD) simulation was applied to assess the binding stability of the top-ranked compound–target complex. Finally, RT-qPCR was conducted on wound edge tissue samples from DFU patients treated with ethacridine to experimentally validate the mRNA expression of predicted hub genes. Results: A total of 302 potential ethacridine-related targets, 4264 DFU-related targets, and 1942 antibacterial-related targets were identified. Intersection analysis revealed 105 common targets potentially involved in the antibacterial effects of ethacridine against DFU. PPI network analysis highlighted 10 hub targets, including AKT1, EGFR, SRC, HSP90AA1, and MMP9. GO enrichment indicated significant involvement in responses to reactive oxygen species, regulation of inflammatory responses, responses to lipopolysaccharide, and bacterial molecular patterns. KEGG pathway analysis identified 157 relevant pathways, including the lipid and atherosclerosis, TNF signaling, IL-17 signaling, and the AGE–RAGE signaling pathways in diabetic complications. Molecular docking demonstrated favorable binding affinities (all < −5.0 kcal/mol) between ethacridine and the hub targets, with the strongest binding observed between MMP9 and ethacridine (−9.8 kcal/mol). These docking results suggest possible interaction tendencies that may contribute indirectly to Ethacridine’s network-level regulatory effects, rather than direct binding to all targets in vivo. Molecular dynamics simulation further confirmed the stable interaction between MMP9 and ethacridine. RT-qPCR validation in clinical DFU tissue samples demonstrated expression trends of key genes consistent with in silico predictions. These results reflect transcriptional regulation consistent with pathway modulation predicted by the network analysis, rather than direct protein–ligand binding across all targets. Conclusion: Ethacridine may exert antibacterial effects against bacterial biofilms in DFU through multi-target and multi-pathway mechanisms. These findings highlight ethacridine’s translational potential as a safe, readily available, and mechanistically validated topical agent for the clinical management of biofilm-associated diabetic foot infections.
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(This article belongs to the Section Bioinformatics and Systems Biology)
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Determination of the Phylogenetic Relationship of Dendrobium linawianum (Orchidaceae) Based on Comparative Analysis of Complete Chloroplast Genomes
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Fengping Zhang, Qiyong Huang, Yaqiong Zhang, Dongqin Lǚ, Rui Chen, Yanshu Jia and Qiongchao Li
Curr. Issues Mol. Biol. 2025, 47(10), 869; https://doi.org/10.3390/cimb47100869 - 21 Oct 2025
Abstract
Dendrobium is an orchid genus with high economic and ecological importance, but its taxonomy based on morphology remains controversial. Dendrobium linawianum, a critically endangered species with both ornamental and medicinal value, represents a key taxon within this genus. However, its phylogenetic relationship
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Dendrobium is an orchid genus with high economic and ecological importance, but its taxonomy based on morphology remains controversial. Dendrobium linawianum, a critically endangered species with both ornamental and medicinal value, represents a key taxon within this genus. However, its phylogenetic relationship has long been unplaced due to similar morphological traits. Despite its conservation and taxonomic importance, its complete chloroplast genome has not been previously characterized. Here, we newly sequenced and assembled the complete chloroplast genome of D. linawianum. The 150,497 bp genome exhibits a typical quadripartite structure, encoding 119 genes. A total of 161 simple sequence repeats (SSRs) were identified, predominantly mononucleotide and dinucleotide motifs. Condon usage analysis revealed leucine as the most abundant amino acid. Phylogenetic analysis based on complete chloroplast genome sequences strongly supported the close relationship of D. linawianum with D. hercoglossum, D. thyrsiflorum, and D. moniliforme, resolving its taxonomic position within the genus. The complete chloroplast genomes successfully resolved the phylogenetic relationships among 35 Dendrobium species, demonstrating their efficacy as powerful molecular markers for resolving taxonomic ambiguities within this morphologically complex genus. Our findings provide a genomic foundation for precise species identification and molecular breeding of D. linawianum, and enhance understanding of phylogenetic relationships in this taxonomically challenging group.
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(This article belongs to the Section Molecular Plant Sciences)
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Neurobiological Correlates of Coping Strategies in PTSD: The Role of IGF-1, CASP-9, nNOS, and IL-10 Based on Brief-COPE Assessment
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Barbara Paraniak-Gieszczyk and Ewa Alicja Ogłodek
Curr. Issues Mol. Biol. 2025, 47(10), 868; https://doi.org/10.3390/cimb47100868 - 21 Oct 2025
Abstract
Post-traumatic stress disorder (PTSD) is associated with long-term disturbances in stress regulation, neuroinflammation, and oxidative stress and reduced psychological coping capacity. The aim of the study was to assess the relationship between selected neurobiological biomarkers (Insulin-like Growth Factor 1—IGF-1; Caspase-9—CASP-9; Neuronal Nitric Oxide
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Post-traumatic stress disorder (PTSD) is associated with long-term disturbances in stress regulation, neuroinflammation, and oxidative stress and reduced psychological coping capacity. The aim of the study was to assess the relationship between selected neurobiological biomarkers (Insulin-like Growth Factor 1—IGF-1; Caspase-9—CASP-9; Neuronal Nitric Oxide Synthase—nNOS; and Interleukin-10—IL-10) and coping styles evaluated using the Brief Coping Orientation to Problems Experienced (Brief-COPE) questionnaire in men with trauma experience. Particular emphasis was placed on analyzing the effect of PTSD chronicity (≤5 years vs. >5 years) on these relationships. The study included 92 adult men with a history of life-threatening situations. Participants were divided into three groups: PTSD within the past ≤5 years (n = 33), PTSD within the past >5 years (n = 31), and a No PTSD group (n = 28). Biomarkers were measured in blood serum. Coping strategies were assessed using the Brief-COPE questionnaire, which includes four subscales: task-oriented, emotion-oriented, avoidant, and general coping. Due to the lack of normal distribution, the Kruskal–Wallis test and Dunn’s post hoc test were used. Correlations between biomarkers and Brief-COPE subscales were calculated using Spearman’s Rank Correlation Coefficient (Rho). Significant differences between groups were found in all four biomarkers (p < 0.001). IGF-1 and IL-10 reached the highest values in the No PTSD group and the lowest in the PTSD ≤ 5 years group, indicating neuroprotective and anti-inflammatory deficits in PTSD. Conversely, CASP-9 and nNOS levels (markers of apoptosis and oxidative stress) were highest in PTSD ≤ 5 years, with partial normalization in the PTSD > 5 years group. In terms of coping strategies, the No PTSD group displayed a highly adaptive profile (task-oriented: 30/32; emotion-oriented: 43/48; and avoidant: 12/32). Individuals with PTSD ≤ 5 years presented a maladaptive pattern (task-oriented: 13/32; avoidant: 26/32; and emotion-oriented: 27/48), while in PTSD > 5 years, a further decline in emotion-oriented (21/48) and general coping (59/112) was observed, suggesting progressive depletion of psychological resources. The strongest correlations between biomarkers and coping strategies occurred in PTSD groups. Low IGF-1 levels in PTSD ≤ 5 years correlated negatively with emotion-oriented coping (Rho = −0.39) and general coping (Rho = −0.35). High CASP-9 levels were associated with reduced task-oriented coping in PTSD > 5 years (Rho = −0.29). Similar trends were observed for nNOS and IL-10, indicating a disturbance in neurobiological balance that favors persistence of PTSD symptoms. PTSD, both in its acute and chronic phases, is associated with an abnormal profile of neuroprotective, apoptotic, and inflammatory biomarkers, which correlates with impaired adaptive coping capacity. Although partial normalization of biological parameters is observed in chronic PTSD, deficits in emotion-oriented and task-oriented coping persist. The Brief-COPE questionnaire, combined with biomarker analysis, may serve as a useful clinical tool for assessing psychophysiological balance and designing early interventions. These results highlight the potential of IGF-1, CASP-9, nNOS, and IL-10 as biomarkers of stress adaptation and therapeutic targets in PTSD.
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(This article belongs to the Section Molecular Medicine)
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Genome-Wide Identification and Functional Evolution of NLR Gene Family in Capsicum annuum
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Chong Feng, Qi Chen, Wenhao Liu, Tengfei Li and Tuo Ji
Curr. Issues Mol. Biol. 2025, 47(10), 867; https://doi.org/10.3390/cimb47100867 - 21 Oct 2025
Abstract
Capsicum annuum (pepper) is a globally significant Solanaceous crop vulnerable to devastating pathogens such as Phytophthora capsici. Nucleotide-binding leucine-rich repeat (NLRs) proteins are crucial intracellular immune receptors mediating effector-triggered immunity (ETI). This study presents the comprehensive genome-wide identification and analysis of the
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Capsicum annuum (pepper) is a globally significant Solanaceous crop vulnerable to devastating pathogens such as Phytophthora capsici. Nucleotide-binding leucine-rich repeat (NLRs) proteins are crucial intracellular immune receptors mediating effector-triggered immunity (ETI). This study presents the comprehensive genome-wide identification and analysis of the NLR gene family in pepper using the high-quality ‘Zhangshugang’ reference genome. We identified 288 high-confidence canonical NLR genes. Chromosomal distribution analysis showed significant clustering, particularly near telomeric regions, with Chr09 harboring the highest density (63 NLRs). Evolutionary analysis demonstrated that tandem duplication is the primary driver of NLR family expansion, accounting for 18.4% of NLR genes (53/288), predominantly on Chr08 and Chr09. Analysis of promoter cis-regulatory elements (CREs) revealed enrichment in defense-related motifs, with 82.6% of promoters (238 genes) containing binding sites for salicylic acid (SA) and/or jasmonic acid (JA) signaling. Transcriptome profiling of Phytophthora capsici-infected resistant (C. annuum cv. CM334) and susceptible (C. annuum cv. NMCA10399) cultivars identified 44 significantly differentially expressed NLR genes, and protein–protein interaction (PPI) network analysis predicted key interactions among them, with Caz01g22900 and Caz09g03820 as potential hubs. This study elucidates the tandem-duplication-driven expansion, domain-specific functional implications, and expression dynamics of the pepper NLR family. It identifies conserved and lineage-specific candidate NLR genes, including Caz03g40070, Caz09g03770, Caz10g20900, and Caz10g21150. These findings provide valuable candidate gene targets for the development of molecular markers for pepper resistance to Phytophthora capsici.
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(This article belongs to the Section Molecular Plant Sciences)
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Comparison of Gut Microbial Structure and Function Changes in Sichuan–Tibetan Black Pigs at Different Growth Stages Based on Metagenomic Analysis
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Lichun Jiang, Yi Qing, Kaiyuan Huang, Huiling Huang, Chengmin Li, Qinggang Mei and Qian Wu
Curr. Issues Mol. Biol. 2025, 47(10), 866; https://doi.org/10.3390/cimb47100866 - 21 Oct 2025
Abstract
The gut microbiota plays a crucial role in maintaining swine health and understanding its stage-specific variations provides a scientific basis for health assessment. This study investigated the structural changes in intestinal microbiota during the development of Sichuan–Tibetan black pigs (n = 15)
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The gut microbiota plays a crucial role in maintaining swine health and understanding its stage-specific variations provides a scientific basis for health assessment. This study investigated the structural changes in intestinal microbiota during the development of Sichuan–Tibetan black pigs (n = 15) by collecting fecal samples at three growth stages: the nursery period (1 month), growing period (3 months), and finishing period (10 months). Microbial profiling was performed using 16S rRNA sequencing. Results showed no significant difference in the Shannon index between the nursery and growing periods, while the finishing period exhibited distinct ACE and Chao 1 indices compared to other stages. PCoA and NMDS analyses revealed significant structural divergence in the finishing period microbiota, with greater intra-group variability observed in the nursery and growing periods. At the phylum level, Firmicutes abundance increased progressively with growth, becoming the absolute dominant phylum, whereas Bacteroidota showed a declining trend. These characteristics are particularly prominent during the finishing period. At the family level, Lactobacillaceae abundance increased continuously. Oscillospiraceae remained stable during the early stages but decreased significantly in the finishing period. Genus-level analysis shows that Lactobacillus, especially L. amylovorus and L. reuteri, become dominant bacterial species during the finishing period. A total of 84 differentially abundant core microbiota were identified, with the finishing period containing the highest number. Functional annotation revealed 19 significantly different metabolic pathways across the three stages. The most significant is the enhanced activity of microorganisms during the finishing period in pathogen-related metabolism and exogenous degradation, reflecting their adaptability to complex feed. These findings demonstrate stage-dependent variations in the gut microbiota of Sichuan–Tibetan black pigs, providing valuable references for nutritional regulation and feeding management practices.
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(This article belongs to the Section Molecular Microbiology)
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Systematic Review: Exosomes as Molecular Messengers in the Development of Obesity-Related Complications in Children
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Kamila Szeliga, Dominika Krakowczyk, Marcin Chyra, Monika Pietrowska, Tomasz Koszutski, Aneta Monika Gawlik-Starzyk and Lidia Hyla-Klekot
Curr. Issues Mol. Biol. 2025, 47(10), 865; https://doi.org/10.3390/cimb47100865 - 20 Oct 2025
Abstract
Emerging evidence highlights extracellular vesicles (EVs), especially exosomes, as critical molecular messengers linking pediatric obesity to multi-organ complications. This scoping review synthesizes current knowledge on EVs-mediated intercellular communication that exacerbates inflammation, insulin resistance, endothelial dysfunction and organ-specific damage. Data demonstrate that adipose- and
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Emerging evidence highlights extracellular vesicles (EVs), especially exosomes, as critical molecular messengers linking pediatric obesity to multi-organ complications. This scoping review synthesizes current knowledge on EVs-mediated intercellular communication that exacerbates inflammation, insulin resistance, endothelial dysfunction and organ-specific damage. Data demonstrate that adipose- and endothelial-derived EVs carry bioactive cargo, microRNAs, proteins, and lipids, that modulate key pathways driving metabolic derangements and vascular injury, often preceding detectable clinical biomarkers. Notably, maternal obesity influences EVs composition in breast milk, shaping early-life metabolic programming and offspring risk of obesity. Recent studies underscore the diagnostic and therapeutic potential of EVs in obesity-related conditions such as metabolic-associated fatty liver disease (MAFLD), early renal injury, and cardiovascular dysfunction in children. Furthermore, EVs released in response to exercise or bariatric surgery may mediate systemic metabolic improvements, offering a novel window into personalized interventions. Despite promising findings, standardization of EV isolation and profiling in pediatric research is lacking, and large-scale longitudinal studies are urgently needed. By deepening our understanding of EVs biology, clinicians may advance early detection, risk stratification, and targeted therapies to interrupt the progression from childhood obesity to lifelong metabolic and cardiovascular disease.
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(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Integrating Multiple Methods to Validate Key Genes Driving the Progression of Breast Ductal Carcinoma In Situ
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Minjie Zhong, Shengkai Zheng, Yahui Wen, Juansi Zhang, Jiahui Zhang, Hanwei Wang, Caiqin Mo, Sunwang Xu and Xiangjin Chen
Curr. Issues Mol. Biol. 2025, 47(10), 864; https://doi.org/10.3390/cimb47100864 - 20 Oct 2025
Abstract
Background: Ductal carcinoma in situ (DCIS) is a precursor to breast cancer. The mechanisms by which the stroma of DCIS affects disease progression remain elusive. Thus, the aim of this study is to identify key stroma genes that affect DCIS progression and to
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Background: Ductal carcinoma in situ (DCIS) is a precursor to breast cancer. The mechanisms by which the stroma of DCIS affects disease progression remain elusive. Thus, the aim of this study is to identify key stroma genes that affect DCIS progression and to define high-risk DCIS cases. Method: Gene expression matrix files from the Gene Expression Omnibus (GEO) database were selected to identify candidate genes associated with the stromal transition from DCIS to invasive ductal carcinoma (IDC). An integrative approach was employed to identify and functionally characterize driver genes of DCIS progression. In vitro experiments were performed to validate the role of these genes. Results: We identified 13 differentially expressed genes (DEGs), of which 5 were selected as candidate drivers. Gene set enrichment analysis (GSEA) revealed the biological functions of RAMP2 and ADM2, while in vitro functional assays demonstrated that ADM2 knockdown and RAMP2 overexpression in breast cancer cell lines significantly suppressed cellular proliferation and invasion. Conclusion: This study identified and validated the roles and functions of ADM2 and RAMP2 and revealed their function as key driver genes in the progression of ductal carcinoma in situ (DCIS). Collectively, our findings elucidate critical genetic mechanisms underlying DCIS progression and provide novel insights for the development of personalized therapeutic strategies.
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(This article belongs to the Section Molecular Medicine)
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Epigenetic Remodeling in Thyroid Cancer: New Dimensions of Targeted Therapy Through lncRNA Modulation
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Adrian Albulescu, Alina Fudulu, Mirela Antonela Mihaila, Iulia Iancu, Adriana Plesa, Marinela Bostan, Anca Botezatu, Lorelei Irina Brasoveanu and Camelia Mia Hotnog
Curr. Issues Mol. Biol. 2025, 47(10), 863; https://doi.org/10.3390/cimb47100863 - 18 Oct 2025
Abstract
Thyroid carcinomas are phenotypically heterogeneous malignancies. Advances in molecular and cellular technologies have revealed genetic, epigenetic, and nongenetic factors underlying this heterogeneity. Our study aimed to assess the impact of single and combined treatments with anticancer agents (Carboplatin, Doxorubicin, Paclitaxel, Avastin), natural compounds
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Thyroid carcinomas are phenotypically heterogeneous malignancies. Advances in molecular and cellular technologies have revealed genetic, epigenetic, and nongenetic factors underlying this heterogeneity. Our study aimed to assess the impact of single and combined treatments with anticancer agents (Carboplatin, Doxorubicin, Paclitaxel, Avastin), natural compounds (Quercetin), and epigenetic modulators (suberoylanilide hydroxamic acid and 5-Azacytidine) on the expression of long noncoding RNAs, methylation regulators, and functional features in the human thyroid cancer cell line K1. Methods: Treated and untreated K1 cells were used throughout experiments to evaluate the drug-induced cytotoxicity, apoptosis, cell cycle distribution, cytokine release, gene expression, and global DNA methylation levels. Results: Some single- and combined-drug treatments modulated both cell cycle progression and apoptotic events, demonstrating anti-tumor activity of the tested compounds. Gene expression analysis showed treatment-specific regulation of target genes and lncRNAs, including both upregulation and downregulation across different drug combinations. All treatments resulted in increased global DNA methylation levels compared to the untreated controls. Several combinations significantly upregulated DNMT1 and DNMT3B, while concomitantly decreased EZH2 levels. Conclusions: These coordinated epigenetic changes highlight the therapeutic potential of combining epigenetic modulators with chemotherapeutic agents, suggesting a strategy to prevent or reverse treatment resistance and improve outcomes in thyroid cancer patients.
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(This article belongs to the Special Issue Molecular Functions of Long Non-Coding RNAs: Implications for Diseases and Therapy)
Open AccessEditorial
Editorial for Special Issue “Mental Disorder: Focus on Pathogenesis to Treatment”
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Fabrizio Bella, Cecilia Chiarenza and Carmen Concerto
Curr. Issues Mol. Biol. 2025, 47(10), 862; https://doi.org/10.3390/cimb47100862 - 18 Oct 2025
Abstract
In recent years, advances in molecular biology have enabled the investigation of previously inaccessible mechanisms at the cellular and immunological levels that underlie the pathogenesis of numerous conditions affecting the central nervous system [...]
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(This article belongs to the Special Issue Mental Disorder: Focus on Pathogenesis to Treatment)
Open AccessArticle
Contributions of Retinoid Signaling to Autism-like Behaviors Induced by Early Postnatal Lead Exposure in the Mouse Cerebellum
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Xiaochun Xia, Xulan Zhou, Zihan Ma, Li Liu, Yaqi Wang, Yongli Wu, Ying Zhang and Juan Wang
Curr. Issues Mol. Biol. 2025, 47(10), 861; https://doi.org/10.3390/cimb47100861 - 18 Oct 2025
Abstract
Autism spectrum disorder (ASD) is a group of neurodevelopmental dysfunctions characterized by a heterogeneous etiology that involves gene–environment interactions. Early postnatal lead (Pb) exposure has been found to be associated with the etiology of ASD, but the mechanisms remain unclear. The present study
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Autism spectrum disorder (ASD) is a group of neurodevelopmental dysfunctions characterized by a heterogeneous etiology that involves gene–environment interactions. Early postnatal lead (Pb) exposure has been found to be associated with the etiology of ASD, but the mechanisms remain unclear. The present study aims to investigate the effects of early Pb exposure on the emergence of ASD-like behaviors in offspring and to evaluate its potential relationship with morphological changes and underlying mechanisms in the cerebellum. The study established a mouse model to study early postnatal Pb exposure and examined ASD-like behaviors through the open field test, novel object recognition test, marble burying test, and three-chamber social test. Quantification of Pb levels was performed in cerebellar tissue, examination of Purkinje cell morphology was carried out, and identification of differential protein expression was conducted using TMT-based quantitative proteomics. The study revealed that the offspring of Pb-exposed mice showed significant social deficits, increased repetitive behaviors, and cognitive impairments. The cerebellum showed both elevated Pb levels and a reduction in Purkinje cells. Proteomic analysis identified 45 proteins that were differentially expressed, showing disruption in the retinoid signaling pathway. These findings demonstrate that early postnatal Pb exposure leads to ASD traits and that retinoid signaling may be a key pathway in the cerebellum, at least in part.
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(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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In Silico Network Pharmacology, Molecular Docking, and Molecular Dynamics Analysis of Rosemary-Derived Compounds as Potential HSP90 Inhibitors for Cancer Therapy
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Radhia Mazri, Mebarka Ouassaf, Afaf Zekri, Shafi Ullah Khan, Kannan R. R. Rengasamy and Bader Y. Alhatlani
Curr. Issues Mol. Biol. 2025, 47(10), 860; https://doi.org/10.3390/cimb47100860 - 18 Oct 2025
Abstract
Cancer remains a major global health challenge, emphasizing the need for new and effective therapies. This study investigates the anticancer potential of bioactive compounds from rosemary (Rosmarinus officinalis) using an integrative network pharmacology and computational approach. Twelve phytochemicals with favorable pharmacological profiles, optimal
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Cancer remains a major global health challenge, emphasizing the need for new and effective therapies. This study investigates the anticancer potential of bioactive compounds from rosemary (Rosmarinus officinalis) using an integrative network pharmacology and computational approach. Twelve phytochemicals with favorable pharmacological profiles, optimal pharmacokinetics, and acceptable toxicological properties were evaluated, revealing 178 putative cancer-related targets. Protein–protein interaction (PPI) analysis highlighted ten key genes—EGFR, ESR1, HIF1A, HSP90AA1, MAPK1, BCL2, STAT3, TP53, CASP3, and SRC—implicated in the progression of various cancers, including breast, colorectal, liver, and lung tumors. Functional enrichment analysis demonstrated their involvement in multiple cancer-associated pathways. Among these, HSP90AA1 emerged as a critical target. Molecular docking revealed Rosmanol, Chlorogenic acid, and Carnosol as the most promising HSP90AA1 binders with strong predicted affinities. ADMET profiling confirmed their excellent drug-likeness and safety profiles, while molecular dynamics simulations validated the stability of the compound–protein complexes, further supporting their potential as HSP90 inhibitors. These findings suggest that rosemary-derived compounds may represent valuable candidates for anticancer drug development, though experimental validation is required to confirm their therapeutic efficacy.
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(This article belongs to the Collection Bioinformatics Approaches to Biomedicine)
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The Linkage Between Inflammation and the Progression of Type 2 Diabetes Mellitus
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Lucy Baldeón-Rojas, Valeria Alulema, Francisco Barrera-Guarderas, Diana Aguirre-Villacís, Cristina Cañadas-Herrera, Ricardo Bedón-Galarza, Francisco Pérez-Tasigchana and Jorge Pérez-Galarza
Curr. Issues Mol. Biol. 2025, 47(10), 859; https://doi.org/10.3390/cimb47100859 - 17 Oct 2025
Abstract
Type 2 diabetes mellitus (T2D) is a chronic metabolic disorder in which inflammation plays a central role in its onset, progression, and complications. Identifying reliable biomarkers is essential to improve risk prediction, disease monitoring, and early intervention. Methods: A total of 169 Ecuadorian
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Type 2 diabetes mellitus (T2D) is a chronic metabolic disorder in which inflammation plays a central role in its onset, progression, and complications. Identifying reliable biomarkers is essential to improve risk prediction, disease monitoring, and early intervention. Methods: A total of 169 Ecuadorian participants were stratified into four clinical groups: non-diabetic controls (NDC), controlled T2D (C-T2D), uncontrolled T2D (NC-T2D), and diabetic kidney disease (DKD). Circulating levels of cytokines (IL-6, IL-8, TNF-α), adipokines (leptin, adiponectin), and PBMC-derived microRNAs (miR-146a, miR-155) were quantified. Associations with disease stage were evaluated using ROC curve analysis and logistic regression. Results: Leptin showed the strongest association with T2D (OR = 13.76, 95% CI: 6.47–29.26), followed by IL-8 (OR = 6.73, 95% CI: 3.30–13.70) and IL-6 (OR = 4.43, 95% CI: 2.26–8.97). Adiponectin distinguished NC-T2D from DKD (OR = 4.15, 95% CI: 1.77–9.71), underscoring its potential as an indicator of renal complications. Interestingly, TNF-α levels declined across disease stages, possibly reflecting subclinical inflammation in Ecuadorian NDC with high rates of obesity and dyslipidemia. PBMC-derived miR-146a was upregulated in T2D patients, contrasting with prior serum-based studies and emphasizing the importance of compartment-specific analysis. miR-155 was elevated in C-T2D, suggesting a compensatory immune-regulatory mechanism that diminishes with poor glycemic control and advanced disease. Conclusions: Inflammatory cytokines, adipokines, and microRNAs act in distinct yet complementary ways in T2D. Leptin, IL-6, and IL-8 emerge as strong predictors of disease, while miR-146a and miR-155 provide additional insight into immune-inflammatory regulation. Integrated biomarker panels may enhance patient stratification and support personalized monitoring of T2D progression.
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(This article belongs to the Section Molecular Medicine)
Open AccessArticle
Pennisetum glaucum (L.) Oral Supplementation Mitigates Multi-Organic Dysfunction Associated with Carcinogenesis in HPV16-Transgenic Mice
by
Paula A. Oliveira, Latifa Hajri, Armando V. Pinto Moreno, Carlos E. Dias Santos, Haissa O. Brito, Margarida M. S. M. Bastos, Rui Medeiros, Soumaya Ghodbane, Mohamed Ammari, Rui M. Gil da Costa and Ana I. Faustino-Rocha
Curr. Issues Mol. Biol. 2025, 47(10), 858; https://doi.org/10.3390/cimb47100858 - 17 Oct 2025
Abstract
Cancers induced by human papillomavirus are often associated with systemic inflammation and cachexia. This study aimed to determine the interference of Pennisetum glaucum oral supplementation over multi-organic dysfunction in HPV16-transgenic mice. The experimental groups included (1) wildtype (WT) mice with standard diet, (2)
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Cancers induced by human papillomavirus are often associated with systemic inflammation and cachexia. This study aimed to determine the interference of Pennisetum glaucum oral supplementation over multi-organic dysfunction in HPV16-transgenic mice. The experimental groups included (1) wildtype (WT) mice with standard diet, (2) WT mice with 36% Pennisetum, (3) transgenic mice with standard diet, (4) transgenic mice with 29% Pennisetum, and (5) transgenic mice with 36% Pennisetum. During the 4-week experimental protocol, body weight, food and water intake, and humane endpoints were recorded. At sacrifice, blood and tissue samples were collected for analysis. Oral supplementation with millet was shown to be safe and well tolerated by both WT and transgenic mice, with no adverse effects on behavior, food or water intake, or general animal welfare. In HPV16-transgenic animals, millet supplementation was associated with an improved health status, reduced serum glucose levels, enhanced antioxidant responses, and a notable reduction in the severity of HPV-induced skin and organ lesions. Overall, Pennisetum glaucum was safe under these experimental conditions and is a promising functional food for patients suffering from systemic paraneoplastic syndromes. Longer exposure periods and doses should be evaluated experimentally before proceeding to clinical trials of Pennisetum-containing diets.
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(This article belongs to the Section Molecular Pharmacology)
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Open AccessArticle
Biphasic Slc2a4 Gene Expression in 3T3-L1 Adipocytes in Response to Treatment with Low and High Concentrations of Daidzein and Genistein
by
Karen Cristina Rego Gregorio, Caroline Pancera Laurindo, Helayne Soares Freitas, Maristela Mitiko Okamoto, Patricia Monteiro Seraphim and Ubiratan Fabres Machado
Curr. Issues Mol. Biol. 2025, 47(10), 857; https://doi.org/10.3390/cimb47100857 - 17 Oct 2025
Abstract
Daidzein and genistein are abundant in soy-rich foods, whose supplementation has been proposed to have beneficial effects on several diseases, including diabetes mellitus and obesity. 17β-estradiol (E2) enhances the expression of the Slc2a4 gene and GLUT4 protein in adipose tissue, increasing glucose consumption
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Daidzein and genistein are abundant in soy-rich foods, whose supplementation has been proposed to have beneficial effects on several diseases, including diabetes mellitus and obesity. 17β-estradiol (E2) enhances the expression of the Slc2a4 gene and GLUT4 protein in adipose tissue, increasing glucose consumption and contributing to glycemic control. We investigated, in 3T3-L1 adipocytes, the effect of low and high doses of daidzein and genistein on Slc2a4/GLUT4 expression and the participation of estrogen receptors 1/2 (ESR1/ESR2) in the regulations observed. Differentiated adipocytes were cultivated, for 24 h, in the presence of 17β-estradiol (E2, 10 nM), daidzein (10 nM–150 μM) and genistein (10 nM–50 μM), with or without ESR1 or ESR2 antagonists. Daidzein/genistein at a low dose (10 nM) increased Slc2a4/GLUT4 expression (50%, p < 0.05), an effect abrogated by an ESR1 antagonist, mimicking the effect of E2. However, maximal doses of daidzein and genistein reduced, in a ESR1-mediated mechanism, the expression of mRNA (by 47% and 60%, p < 0.001) and the protein (by 29% and 36%, p < 0.01), respectively, for daidzein and genistein, as compared to E2. In conclusion, in adipocytes, daidzein and genistein have a biphasic ESR1-mediated effect: while low concentrations increase the expression of Slc2a4/GLUT4, high concentrations decrease it, the former predisposing to an adipogenic effect, the latter to a diabetogenic condition.
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(This article belongs to the Special Issue Molecular Insights into Food-Derived Natural Products and Their Biological Activities—2nd Edition)
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Open AccessArticle
GPX4 Inhibition Enhances the Pro-Oxidant and ER Stress Effects of Tempol in Colon and Gastric Cancer Cell Lines
by
Gorkem Ozdemir and Halil Mahir Kaplan
Curr. Issues Mol. Biol. 2025, 47(10), 856; https://doi.org/10.3390/cimb47100856 - 16 Oct 2025
Abstract
Tempol, a synthetic nitroxide, exhibits dual antioxidant and pro-oxidant activity, requiring millimolar concentrations to induce oxidative stress, which limits its therapeutic use. Glutathione Peroxidase 4 (GPX4) is a critical lipid peroxidase that prevents ferroptosis, and its inhibition has emerged as a strategy to
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Tempol, a synthetic nitroxide, exhibits dual antioxidant and pro-oxidant activity, requiring millimolar concentrations to induce oxidative stress, which limits its therapeutic use. Glutathione Peroxidase 4 (GPX4) is a critical lipid peroxidase that prevents ferroptosis, and its inhibition has emerged as a strategy to sensitize cancer cells to oxidative stress. To enhance Tempol’s efficacy, we investigated its interaction with ML210, a GPX4 inhibitor, in human colon (HT29) and gastric (CRL-1739) cancer cell lines. We quantified cell viability, oxidative stress markers (H2O2, Total Oxidant Status (TOS), and Total Antioxidant Status (TAS)) and endoplasmic reticulum (ER) stress proteins (ATF6, GRP78, and IRE1α) in in vitro assays. Synergy was assessed using Bliss independence analysis. The combination of Tempol (2 mM) and ML210 (0.05 μM) markedly reduced viability in both cell lines. Bliss analysis revealed slight/moderate synergy for cytotoxicity (Δ = +0.15 in HT29; Δ = +0.26 in CRL-1739) and strong synergy for H2O2 accumulation (Δ = +1.92–2.23 across replicates). In contrast, TOS showed moderate-to-strong antagonism across both cell lines, and TAS demonstrated slight synergistic or antagonistic effects. ER stress markers exhibited marker and cell line specific synergy: ATF6 showed strong synergy, IRE1α slight synergy in both lines, and GRP78 activation was highly variable, showing strong synergy in CRL-1739 cells but moderate antagonism in HT29 cells. These findings indicate that the cooperative action of Tempol and ML210 is ROS-pool–specific and pathway-selective in the ER. These findings demonstrate that ML210 potentiates Tempol’s pro-oxidant pressure by targeting GPX4, selectively amplifying H2O2 accumulation and ER stress engagement without collapsing global redox balance. This study provides mechanistic rationale for redox–proteostasis co-targeting in gastric and colon cancers and establishes a foundation for in vivo validation.
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(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Open AccessReview
Epigenetic Mechanisms in Fabry Disease: A Thematic Analysis Linking Differential Methylation Profiles and Genetic Modifiers to Disease Phenotype
by
Jatinder Singh, Paramala Santosh and Uma Ramaswami
Curr. Issues Mol. Biol. 2025, 47(10), 855; https://doi.org/10.3390/cimb47100855 - 16 Oct 2025
Abstract
Background/Objectives: Fabry disease is an X-linked lysosomal storage disorder. It is characterised by impaired metabolism of glycosphingolipids whose accumulation causes irreversible organ damage and life-threatening complications. Genotype–phenotype correlations have a limited scope in Fabry disease as the disorder presents with wide-ranging
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Background/Objectives: Fabry disease is an X-linked lysosomal storage disorder. It is characterised by impaired metabolism of glycosphingolipids whose accumulation causes irreversible organ damage and life-threatening complications. Genotype–phenotype correlations have a limited scope in Fabry disease as the disorder presents with wide-ranging clinical variability. In other X-linked disorders, epigenetic profiling has identified methylation patterns and disease modifiers that may explain clinical heterogeneity. In this narrative review and thematic analysis, the role of DNA methylation and epigenetics on the clinical phenotype in Fabry disease was investigated. Methods: Embase, PubMed, and PsycINFO were searched to identify literature on DNA methylation and epigenetics in Fabry disease. Based on the eligibility criteria, 20 articles were identified, and a thematic analysis was performed on the extracted data to identify themes. Results: Three themes emerged: (I) genetic modifiers, (II) methylation profiling, and (III) insights into X chromosome inactivation (XCI). The evidence synthesis revealed that telomere length, especially in early disease stages, bidirectional promoter (BDP) methylation by sphingolipids, epigenetic reader proteins, mitochondrial DNA haplogroups, and DNA methylation of the promoter region of the calcitonin receptor gene are potential genetic modifiers in Fabry disease. Methylation patterns also reveal episignatures in Fabry disease evolution and genes implicated in the maintenance of basement membranes. Studies on XCI further emphasise disease heterogeneity and draw attention to methodological issues in the assessment of XCI. Conclusions: This thematic review shows that DNA methylation and genetic modifiers are key factors modifying clinical variability in Fabry disease. More broadly, it underscores a crucial role for epigenetic processes in driving disease onset, progression, and severity in X-linked disorders.
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(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2025)
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Open AccessReview
Pathophysiological Links Between Stroke and Prediabetes: A Systematic Review
by
Yerushka Naicker and Andile Khathi
Curr. Issues Mol. Biol. 2025, 47(10), 854; https://doi.org/10.3390/cimb47100854 - 16 Oct 2025
Abstract
Prediabetes is an intermediate stage between normoglycaemia and type 2 diabetes mellitus (T2DM), affecting over 425 million people globally and contributing to vascular damage and increased stroke risk. Despite the severity of both conditions, their association remains underexplored. This review examines the literature
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Prediabetes is an intermediate stage between normoglycaemia and type 2 diabetes mellitus (T2DM), affecting over 425 million people globally and contributing to vascular damage and increased stroke risk. Despite the severity of both conditions, their association remains underexplored. This review examines the literature on stroke-related biomarkers in normoglycaemia, prediabetes and T2DM to identify potential links between prediabetes and stroke. This systematic review followed PRISMA-2020 guidelines. PubMed, Google Scholar, Scopus, Web of Science and Science Direct were searched for studies (2003–2023) on stroke biomarkers in prediabetes. Eligible studies were original human research in English, with defined diagnostic criteria (ADA or WHO) for glycaemic status and reported biomarker associations or stroke risk. Studies with major comorbidities were excluded. Data were extracted and bias was assessed using the Newcastle–Ottawa Scale. Meta-analysis was not performed due to limited studies per biomarker. Eight studies (n = 3003) were included. NSE was examined in three studies, all reporting significant elevations in hyperglycaemic individuals. Interleukin-6 (IL-6) was assessed in two studies; one showed a significant increase in diabetes, while the other found a non-significant upward trend. D-dimer and GFAP were each reported in separate single studies, both showing significant elevations in hyperglycaemic individuals with stroke or neurocognitive impairment. S100B was investigated in two studies, with divergent findings: one showed a positive association with glycaemic status, while the other reported lower levels in hyperglycaemia. Findings indicate biomarker alterations in T2DM, suggesting that early changes may occur in prediabetes. Our review suggests that individuals with prediabetes may show alterations in inflammatory (IL-6), coagulation (D-dimer), and neurovascular (S100B, GFAP, NSE) markers, though some findings are inconsistent, reflecting early pathophysiological changes that may increase stroke risk. Further well-designed studies are needed to clarify these associations and establish biomarker-based tools for earlier stroke risk detection and prevention in individuals with prediabetes.
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(This article belongs to the Special Issue Cerebrovascular Diseases: From Pathogenesis to Treatment)
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Open AccessReview
The Pathogenesis of Chronic Kidney Disease (CKD) and the Preventive and Therapeutic Effects of Natural Products
by
Yuxin Dong and Yanqing Tong
Curr. Issues Mol. Biol. 2025, 47(10), 853; https://doi.org/10.3390/cimb47100853 - 16 Oct 2025
Abstract
Chronickidney disease (CKD) poses a major global public health challenge, driven by a complex pathogenesis involving multiple interconnected processes—including metabolic disturbances, chronic inflammation, oxidative stress, endoplasmic reticulum stress, and ferroptosis—which collectively contribute to progressive and often irreversible loss of renal function. Although current
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Chronickidney disease (CKD) poses a major global public health challenge, driven by a complex pathogenesis involving multiple interconnected processes—including metabolic disturbances, chronic inflammation, oxidative stress, endoplasmic reticulum stress, and ferroptosis—which collectively contribute to progressive and often irreversible loss of renal function. Although current standard therapies can ameliorate CKD progression, a substantial number of patients still advance to end-stage renal disease, highlighting the urgent need for innovative treatment strategies. Natural products have shown great promise in the prevention and management of CKD, largely attributable to their multi-target and multi-pathway synergistic effects. This review systematically outlines the core pathogenic mechanisms underlying CKD and elucidates the molecular mechanisms through which bioactive natural compounds exert renoprotective effects. Despite robust preclinical evidence, the clinical translation of these compounds remains hindered by limitations such as poor bioavailability and a lack of large-scale clinical trials. Moving forward, research should prioritize clinical translation of these compounds, aiming to provide novel therapeutic perspectives for CKD management.
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(This article belongs to the Special Issue Applications of Natural and Pseudo-Natural Products in Drug Discovery and Development 2025)
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