Epigenomes最新文献

{"title":"GPX Knockdown Is Associated with Altered Redox Homeostasis, Plant Development, and DNA Methylation-Related Profiles in Rice.","authors":"Pedro Alexander Velasquez-Vasconez, Marina de Lima Nogueira, Carlos Betancourth García, Claudia Elizabeth Salazar-González, Angie Fernanda Riascos-España","doi":"10.3390/epigenomes10030049","DOIUrl":"10.3390/epigenomes10030049","url":null,"abstract":"<p><strong>Background: </strong>Glutathione peroxidases (GPXs) regulate peroxide detoxification and redox signaling, but their relationship with DNA methylation remains unclear in Oryza sativa. This study evaluated whether silencing mitochondrial GPX1 and GPX3 is associated with changes in growth, antioxidant activity, and DNA methylation-related profiles.</p><p><strong>Methods: </strong>Non-transformed plants (NT) and five GPX-silenced lines were evaluated in a randomized complete block design. Morphophysiological traits, antioxidant enzyme activities, total 5-methylcytosine content, and methylation-sensitive restriction profiles were analyzed.</p><p><strong>Results: </strong>GPX silencing impaired early establishment and significantly affected flowering time and leaf, root, seed, and total biomass. Total dry biomass decreased by 62.1% in the most affected GPX1 lines and by 29.2% in GPX3 lines relative to NT plants. Root biomass declined by up to 86.1%, and flowering was delayed by up to 30.7 days. Genotype significantly affected GPX-associated and glutathione reductase activities, whereas no significant genotype effects were detected for catalase, ascorbate peroxidase, or superoxide dismutase activities. GPX-associated and glutathione reductase activities were strongly correlated (r = 0.85, <i>p</i> < 0.001), consistent with selective alteration of GPX-associated and glutathione-linked redox metabolism. Total 5-methylcytosine content decreased by 41-42% in GPX-silenced groups. However, increased McrBC digestion and unchanged HpaII/MspI profiles indicated that methylation-related changes were nonuniform and depended on the genomic sites recognized by each enzymatic assay.</p><p><strong>Conclusions: </strong>These findings show that mitochondrial GPX knockdown is associated with impaired rice growth and reproductive development, as well as with altered total 5-methylcytosine content and restriction-sensitive methylation profiles, suggesting a potential relationship among redox homeostasis, developmental regulation, and epigenetic plasticity that requires further validation using locus-resolved and mechanistic approaches.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13510893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148834758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolution of Epigenetic Regulation in Plant Reproduction.","authors":"Vladimir Brukhin","doi":"10.3390/epigenomes10030048","DOIUrl":"10.3390/epigenomes10030048","url":null,"abstract":"<p><p>Epigenetic regulation has played a fundamental role in the evolution of plant reproduction. Across more than a billion years, ancestral genome-defense mechanisms in early eukaryotes were progressively expanded, diversified, and repurposed throughout the green lineage. Streptophyte algae assembled the first plant-specific methylation and small RNA systems, providing pre-adaptations for terrestrial reproduction. In bryophytes and early vascular plants, these systems became integrated into gametophyte development, sporogenesis, and meiotic genome protection. Seed plants experienced substantial diversification and expansion of chromatin regulators and small RNA machinery, enabling increasingly sophisticated control of cone, ovule, and embryo development. Angiosperms underwent the most dramatic rewiring of epigenetic pathways, including gene-family diversification, subfunctionalization, and the emergence of genomic imprinting, endosperm-specific demethylation, and lineage-specific reproductive small RNAs such as phasiRNAs. Convergent solutions, including imprinting, meiotic transposable element (TE) silencing, and TE-derived regulatory elements, arose independently across lineages. Rather than reflecting the emergence of entirely new molecular machinery, these innovations illustrate repeated functional co-option and regulatory rewiring of deeply conserved epigenetic modules. Ecological and life-history pressures further shaped epigenetic diversification, linking environmental stress, mating systems, and domestication to reproductive epigenetic plasticity. Recent evidence further demonstrates that epigenetic plasticity underlies the recurrent evolution of alternative reproductive strategies such as apomixis and contributes to reproductive responses to environmental stress. Advances in comparative epigenomics, single-cell technologies, and epigenome editing are now providing unprecedented opportunities to reconstruct the evolutionary history of reproductive epigenetic pathways and to harness them for crop improvement. Together, these findings reveal epigenetic regulation as a dynamic, modular, and deeply evolvable framework that has repeatedly enabled reproductive innovation throughout plant evolution.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of MicroRNA Expression Levels in Peripheral Blood of Turkish Males with Cocaine Use Disorder.","authors":"Süheyla Ayfer Arslan, Selda Mercan, Günay Çetin, Hasan Mırsal","doi":"10.3390/epigenomes10030047","DOIUrl":"10.3390/epigenomes10030047","url":null,"abstract":"<p><p><b>Background:</b> It is observed that there are a limited number of scientific studies investigating the effect of cocaine use disorder on microRNA (miRNA) levels in human peripheral blood. This study aimed to identify candidate miRNAs that may play a role in the regulation of cocaine addiction by detecting changes in the expression of some miRNAs (miR-9-5p, miR-26b-5p, miR-132-3p, and miR-134-5p) in the peripheral whole blood of cocaine addicts. <b>Methods:</b> Peripheral blood samples were collected from 12 Turkish male individuals with cocaine abuse, 11 Turkish male individuals undergoing treatment for cocaine abuse, and 16 healthy Turkish male individuals without any substance abuse. The change in the expression of microRNAs was determined by quantitative real-time polymerase chain reaction (RT-qPCR). In statistical analyses, ΔCt values were analyzed for the expression of miRNAs. Receiver operating characteristic (ROC) analysis was used to assess the diagnostic adequacy of peripheral blood miRNAs. <b>Results:</b> miR-132-3p and miR-134-5p were downregulated in the addict group compared to the control group (<i>p</i> < 0.05). The areas under the curves (AUCs) of the ROC curve of miR-132-3p and miR-134-5p were significant at 0.778 and 0.744, respectively. <b>Conclusions:</b> This study suggests that miR-132-3p and miR-134-5p may have function as therapeutic markers in the treatment of cocaine use disorder.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13397856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paternal Methionine Supplementation Alters DNA Methylation Patterns in Preimplantation Sheep Embryos.","authors":"Jessica Townsend Graybeal, Zeynep Kizilaslan, Mehmet Kizilaslan, Todd Taylor, Hasan Khatib","doi":"10.3390/epigenomes10030046","DOIUrl":"10.3390/epigenomes10030046","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Parental environmental factors can shape developmental outcomes through epigenetic mechanisms that regulate gene expression. While maternal dietary effects on offspring epigenetics have been well characterized, the impact of paternal diet on embryonic DNA methylation remains poorly understood. Here, we investigated the effect of paternal methionine supplementation on DNA methylation patterns in preimplantation embryos in Polypay sheep. <b>Methods:</b> Four yearling rams (two control and two methionine-supplemented) were bred to twelve ewes following estrus synchronization and superovulation. Embryos were collected after natural mating and analyzed using whole-genome bisulfite sequencing (WGBS). <b>Results:</b> A total of 842 differentially methylated cytosines (DMCs) were identified in embryos derived from methionine-supplemented sires compared to controls, with 835 hypermethylated and 7 hypomethylated. The majority of DMCs were located in intergenic regions, with minimal representation in exonic regions. To assess overlap between parental dietary effects, DMCs identified in this study were compared with those previously reported in embryos derived from methionine-supplemented dams. Eight hypermethylated DMCs were shared between the two datasets, while no hypomethylated DMCs overlapped. To evaluate the functional relevance of differentially methylated genes, we performed siRNA-mediated knockdown of <i>SSU72</i>, a gene associated with multiple DMCs. Knockdown of <i>SSU72</i> resulted in an average 18% decrease in blastocyst formation rate (<i>p</i> < 0.001). <b>Conclusions:</b> These results demonstrate that paternal methionine supplementation alters embryonic DNA methylation patterns and that affected genes may play critical roles in early embryonic development, contributing to fetal programming.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic Mechanisms of Breast and Ovarian Cancer Development: Interplay Between DNA Methylation/Demethylation Enzymes, MicroRNAs, and Long Non-Coding RNAs.","authors":"Svetlana S Lukina, Irina V Pronina, Alexander A Bril, Alexey M Burdennyy, Vitaly I Loginov, Sergey G Morozov","doi":"10.3390/epigenomes10030045","DOIUrl":"10.3390/epigenomes10030045","url":null,"abstract":"<p><p>Structural and functional disruptions of the epigenome are hallmarks of breast and ovarian carcinogenesis. This review dissects the reciprocal regulatory networks co-operated by DNA methyltransferases (DNMTs), ten-eleven translocation enzymes (TETs), and key non-coding RNAs (microRNAs and lncRNAs). We map the precise molecular mechanisms through which these epigenetic modulators alter chromatin accessibility, drive transcriptional reprogramming, and promote phenotypic plasticity in hormone-dependent malignancies. By systematically contrasting the distinct yet overlapping epigenetic profiles of breast and ovarian tumors, we elucidate how these aberrations dictate clinical outcomes. This comprehensive synthesis offers critical insights into the dual utility of these epigenetic elements as dual-purpose diagnostic biomarkers and druggable therapeutic targets, laying the groundwork for next-generation targeted epigenetical therapies.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dose-Dependent Genome-Wide DNA Methylation Remodeling by Metformin Modulates Doxorubicin Sensitivity in Cardiac Cells.","authors":"Mahmoud Abu Shayeb, Nagham N Hendi, Georges Nemer, Hana Hammad, Malek Zihlif, Heba Saadeh, Heba Mansour","doi":"10.3390/epigenomes10030044","DOIUrl":"10.3390/epigenomes10030044","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Doxorubicin (DOX) is an effective chemotherapeutic agent, but its clinical use is limited by dose-dependent cardiotoxicity. Emerging evidence suggests that epigenetic dysregulation, particularly altered DNA methylation, contributes to DOX-induced cardiac injury. Metformin has been reported to exert cardiometabolic and epigenetic regulatory effects. This study investigated genome-wide DNA methylation changes induced by chronic metformin exposure and their effects on doxorubicin sensitivity in H9c2 cardiomyoblast cells. <b>Methods:</b> Genome-wide DNA methylation changes induced by chronic metformin exposure were investigated in H9c2 cardiomyoblast cells using whole-genome bisulfite sequencing (WGBS). Cells were treated with metformin (0.7-2.8 mM) for four months prior to DOX exposure. Cellular sensitivity to DOX was evaluated using MTT-based dose-response analysis and IC₅₀ estimation. <b>Results:</b> DOX reduced cell viability (IC₅₀ = 0.164 µM). Chronic metformin pre-treatment produced a dose-dependent rightward shift in DOX dose-response curves, increasing IC₅₀ values to 0.21, 0.289, and 0.51 µM at 0.7, 1.4, and 2.8 mM metformin, respectively. WGBS revealed distinct separation between treatment groups in principal component analysis. Significant methylation changes (adjusted <i>p</i>-value < 0.05) were identified in genes related to oxidative stress, mitochondrial function, apoptosis, and chromatin regulation. <b>Conclusions:</b> Chronic metformin exposure induces dose-dependent genome-wide DNA methylation remodeling in cardiac cells and is associated with altered cellular sensitivity to doxorubicin. These findings suggest that metabolic modulation by metformin may influence epigenetic regulation and cellular stress responses relevant to chemotherapy-induced cardiotoxicity.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of X-Chromosome Inactivation in Pathogenesis of Turner Syndrome.","authors":"Ana-Maria Grigore, Lavinia Caba, Vlad Teodor Iacob, Lucian-Mihai Antoci, Monica Cristina Pânzaru, Lăcrămioara Ionela Butnariu, Eusebiu Vlad Gorduza","doi":"10.3390/epigenomes10030043","DOIUrl":"10.3390/epigenomes10030043","url":null,"abstract":"<p><p>Turner syndrome (TS), a disorder caused by the complete or partial absence of an X chromosome, exhibits significant clinical variability that cannot be fully explained by chromosomal anomalies alone. This narrative review highlights the crucial role of epigenetic mechanisms, particularly X-chromosome inactivation (XCI), in shaping the TS phenotype. The haploinsufficiency of genes that normally escape XCI is a primary driver of TS features. The specific epigenetic consequences depend on the chromosomal anomaly. In complete monosomy (45,X), the absence of escape-mediated dosage compensation genes from a second X chromosome amplifies haploinsufficiency across X-linked escape genes. Isochromosome Xq (i(Xq)) variants involve the loss of the short arm (Xp) and duplication of the long arm (Xq), creating a dual dosage imbalance with extreme XCI skewing. Carriers of i(Xq) also have a heightened risk for autoimmune disorders compared to those with 45,X TS. For ring-X chromosomes (r(X)), which are mitotically unstable, the functional status of the <i>XIST</i> gene is critical. If the ring is <i>XIST</i>-negative, it remains transcriptionally active, resulting in functional disomy and a more severe phenotype with pronounced neurodevelopmental and craniofacial features. Ultimately, the clinical heterogeneity in TS arises from a complex interplay of the specific chromosomal structure, tissue-specific mosaicism, <i>XIST</i> function, and variable escape from XCI, defining TS as a disorder of epigenetic and gene-regulatory imbalance. However, future research requires a better understanding of the complex mechanism of X-chromosome inactivation.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398325/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vigorous Physical Activity Mitigates Susceptibility to Obesity Associated with Risk Genotypes of <i>FTO</i> and <i>MC4R</i>, and <i>SREBF1</i> Is Hypermethylated: A Cross-Sectional Pilot Study.","authors":"Jenni Chambers, Mary Erazo Bastidas, Clare M P Roscoe, Corinna Chidley, Aaisha Makkar, Aparna Duggirala","doi":"10.3390/epigenomes10020042","DOIUrl":"10.3390/epigenomes10020042","url":null,"abstract":"<p><p><b>Aim</b>: The aim of this study was to correlate single-nucleotide polymorphisms (SNPs) in the <i>FTO</i> and <i>MC4R</i> genes with body composition (BC) in populations with various levels of physical activity, and to investigate associations of <i>SREBF1</i> methylation with the level of physical activity (PA) and BC. <b>Methods</b>: Fifty-six participants aged 18-65 years old with no underlying medical conditions were included in the study and were classified into sedentary/light PA (SLPA), moderate PA (MPA) and vigorous PA (VPA) groups using the International PA questionnaire (IPAQ). Anthropometric measures such as age, gender, body mass index (BMI) and body fat percentage (BFP) were recorded at the time of recruitment. Venous blood samples were collected during participant recruitment and DNA was extracted. Genotyping assays were performed for SNPs in <i>FTO</i> (rs9939609) and <i>MC4R</i> (rs17782313) using Taqman^® RT qPCR and TaqMan Genotyper software 1.7.1. Methylation analysis assay for CpG sites in the <i>SREBF1</i> gene was performed on 56 samples using PyroMark^® Q48 Autoprep (Qiagen, Venlo, The Netherlands). The results were statistically analysed to identify any associations between <i>FTO</i>/<i>MC4R</i> genotypes and the level of PA, and between <i>SREBF1</i> methylation status and the level of PA. This is the first study to investigate links between PA and quantitative methylation of <i>SREBF1</i>. <b>Results</b>: According to IPAQ guidance, the 56 participants were classified into SLPA <i>n</i> = 14, MPA <i>n</i> = 11 and VPA <i>n</i> = 31. The correlation analysis revealed that the <i>FTO</i> rs9939609 'A' risk allele had a significant negative association with BFP in the VPA group (<i>p</i> = 0.0387); the <i>MC4R</i> rs17782313 'C' risk allele had a significant positive association with BMI in the VPA group (<i>p</i> = 0.0256). In the <i>SREBF1</i> pyrosequencing analysis, higher levels of methylation were observed in the VPA group (<i>p</i> = 0.07). <b>Conclusions</b>: We concluded that SNPs associated with obesity identified in <i>FTO</i> rs9939609 and <i>MC4R</i> rs17782313 could help to predict the molecular effects of PA. A high frequency of <i>FTO</i> risk variants in the cohort was observed and the VPA group could help maintain a healthy BFP.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 2","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13297707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148320696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Remodelling of miRNA Regulatory Landscape During West Nile Virus (WNV) Infection.","authors":"Lachlan De Hayr, Alexander A Khromykh, Andrii Slonchak","doi":"10.3390/epigenomes10020041","DOIUrl":"10.3390/epigenomes10020041","url":null,"abstract":"<p><p><b>Background/Objectives:</b> West Nile virus (WNV) remains a significant threat to human health, with no approved antiviral treatments or vaccine available. A better understanding of the molecular mechanisms governing flavivirus-host interactions is needed to identify host regulatory pathways involved in infection. This study aimed to investigate how WNV infection remodels the host miRNA-mRNA regulatory landscape. <b>Methods:</b> WNV-induced changes in host miRNA expression in HEK-293 cells were profiled using miRNA-Seq. Transcriptome-wide host gene expression changes in WNV-infected cells were analysed using RNA-Seq. Gene Ontology and pathway enrichment analyses were conducted using DAVID. Integrated miRNA-mRNA network reconstruction was performed using Cytoscape based on the experimentally validated miRNA-mRNA interactions in miRNet database. <b>Results:</b> WNV infection induced global changes in host miRNA expression, with pathogenic NY99 and non-pathogenic Kunjin strains of the virus producing overlapping and strain-specific alterations in the miRNA landscape. Transcriptome analysis showed strong induction of interferon-related responses and activation of NF-κB and MAPK signalling pathways in the infected cells. In contrast, pathways associated with RNA processing, splicing, and proteasomal degradation were downregulated. Integrated miRNA-mRNA network analysis identified miR-197-3p, miR-301b-3p, miR-129-3p, miR-3662, and miR-128-5p as candidate regulatory hubs involved in WNV-induced transcriptome remodelling. These networks suggested that miRNA-mediated regulation may influence antiviral signalling, apoptosis, and RNA metabolism during infection. <b>Conclusions:</b> These findings suggest that WNV infection broadly remodels host miRNA-mRNA regulatory networks and identifies candidate miRNAs that may contribute to the regulation of antiviral and cellular stress responses. These predicted regulatory interactions provide a foundation for future experimental validation.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 2","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13298079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148320665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Epigenetics in Corneal Fibrosis.","authors":"Julia T Coelho, Ella J Dewald, Syeda R Ali, Moira L Geary, Mithun Santra, Gary H F Yam","doi":"10.3390/epigenomes10020040","DOIUrl":"10.3390/epigenomes10020040","url":null,"abstract":"<p><p>Epigenetics regulates gene activity without altering the underlying DNA sequences. Numerous studies have highlighted the importance of epigenetics in diverse physiological processes, including cell growth, differentiation, and tissue development. Increasingly, epigenetic modifications are recognized for their involvement in various diseases, notably corneal disorders. Corneal fibrosis, a common consequence of ocular injury or infection, significantly contributes to visual impairment and blindness worldwide. Recent evidence indicates that epigenetic changes regulate key processes in corneal pathogenesis, such as inflammation, wound healing, extracellular matrix remodeling, fibrosis, and neovascularization. These findings underscore the potential of developing novel therapeutic strategies that specifically target epigenetic mechanisms to treat or mitigate corneal pathology. Nevertheless, bringing epigenetic therapies into clinical practice remains challenging given the complexity of epigenetic regulation. Future research leveraging multi-omics technologies and specific gene manipulation will be essential to elucidate the mechanisms underlying epigenetic regulation in corneal diseases and to identify specific therapeutic targets. Such advancements will drive the development of effective, clinically relevant treatments for corneal fibrosis and related disorders.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"10 2","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13298491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148320673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}