Epigenomes最新文献

{"title":"The Effect of Clinical Factors on the Reversion of Cg05575921 Methylation in Smoking Cessation.","authors":"Robert Philibert, Steven R H Beach, Michelle R vanDellen, James A Mills, Jeffrey D Long","doi":"10.3390/epigenomes9020012","DOIUrl":"10.3390/epigenomes9020012","url":null,"abstract":"<p><strong>Background: </strong>Financial Incentive Treatments (FIT) can be effective in the treatment of smoking. However, weaknesses in current biochemical approaches for assessing smoking cessation may hinder its implementation, particularly for management of long-term smoking cessation. The use of cg05575921 methylation assessments could address some of the shortcomings of current self-report and non-self-report methods, but additional information is needed about the speed of methylation reversion as a function of key clinical and demographic variables.</p><p><strong>Methods: </strong>To better understand those relationships, we analyzed data from 3040 subjects from the National Lung Screening Trial (NLST), including 1552 self-reported quitters.</p><p><strong>Results: </strong>Plotting of the data as a function of time since quitting shows that methylation increases approximately 14%, on average, after at least one full year of cessation with a subsequent slow non-linear increase in methylation over the next 14 years. Least Squares Regression modeling shows strong effects of quit time and a modest, yet significant, effect of body mass index (BMI) on the rate of reversion. Prior cigarette consumption characteristics and sex made modest contributions as well, with the latter largely offset by pre-cessation methylation levels. Race and age were not significant factors in the models.</p><p><strong>Conclusions: </strong>When combined with data from prior studies, these analyses of the long-term reversion of cg05575921 methylation will be informative to those considering FIT approaches to incentivizing reversion of cg05575921 as an index of short- and long-term smoking cessation.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144129367","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":"Induction of DNA Demethylation: Strategies and Consequences.","authors":"Pietro Salvatore Carollo, Viviana Barra","doi":"10.3390/epigenomes9020011","DOIUrl":"https://doi.org/10.3390/epigenomes9020011","url":null,"abstract":"<p><p>DNA methylation is an important epigenetic modification with a plethora of effects on cells, ranging from the regulation of gene transcription to shaping chromatin structure. Notably, DNA methylation occurs thanks to the activity of DNA methyltransferases (DNMTs), which covalently add a methyl group to the cytosine in position 5' in CpG dinucleotides. Different strategies have been developed to study the effects of DNA methylation in cells, involving either DNMTs inhibition (passive DNA demethylation) or the use of Ten-eleven translocation protein (TET) family enzymes, which directly demethylate DNA (active DNA demethylation). In this manuscript, we will briefly cover the most commonly used strategies in the last two decades to achieve DNA demethylation, along with their effects on cells. We will also discuss some of the newest inducible ways to inhibit DNMTs without remarkable side effects, as well as the effect of non-coding RNAs on DNA methylation. Lastly, we will briefly examine the use of DNA methylation inhibition in biomedical research.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144059361","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 Good, the Bad, and the Epigenetic: Stress-Induced Metabolite Regulation and Transgenerational Effects.","authors":"Saida Ibragić, Sabina Dahija, Erna Karalija","doi":"10.3390/epigenomes9020010","DOIUrl":"https://doi.org/10.3390/epigenomes9020010","url":null,"abstract":"<p><strong>Background: </strong>Plants face a wide range of environmental stresses that disrupt growth and productivity. To survive and adapt, they undergo complex metabolic reprogramming by redirecting carbon and nitrogen fluxes toward the biosynthesis of protective secondary metabolites such as phenylpropanoids, flavonoids, and lignin. Recent research has revealed that these stress-induced metabolic processes are tightly regulated by epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs.</p><p><strong>Methods: </strong>This review synthesizes current findings from studies on both model and crop plants, examining the roles of key epigenetic regulators in controlling secondary metabolism under stress. Special focus is placed on dynamic changes in DNA methylation, histone acetylation, and the action of small RNAs such as siRNAs and miRNAs in transcriptional and post-transcriptional regulation.</p><p><strong>Results: </strong>Evidence indicates that stress triggers rapid and reversible epigenetic modifications that modulate gene expression linked to secondary metabolic pathways. These modifications not only facilitate immediate metabolic responses but can also contribute to stress memory. In some cases, this memory is retained and transmitted to the next generation, influencing progeny stress responses. However, critical knowledge gaps remain, particularly concerning the temporal dynamics, tissue specificity, and long-term stability of these epigenetic marks in crops.</p><p><strong>Conclusions: </strong>Understanding how epigenetic regulation governs secondary metabolite production offers promising avenues to enhance crop resilience and productivity in the context of climate change. Future research should prioritize dissecting the stability and heritability of these modifications to support the development of epigenetically informed breeding strategies.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144059374","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 Association of Childhood Allergic Diseases with Prenatal Exposure to Pollen Grains Through At-Birth DNA Methylation.","authors":"Rajesh Melaram, Hongmei Zhang, James Adefisoye, Hasan Arshad","doi":"10.3390/epigenomes9010009","DOIUrl":"10.3390/epigenomes9010009","url":null,"abstract":"<p><strong>Background: </strong>Pollen exposure in early life is shown to be associated with allergy and asthma. DNA methylation (DNAm), an epigenetic marker, potentially reacts to pollen. However, the role of at-birth DNAm between prenatal pollen grain (PPG) exposure and childhood asthma and allergic rhinitis is unknown.</p><p><strong>Methods: </strong>Data in a birth cohort study on the Isle of Wight, UK, were analyzed (<i>n</i> = 236). Newborn DNAm was measured in cord blood or blood spots on Guthrie cards and screened for potential association with PPG exposure using the R package ttScreening. CpGs that passed screening were further assessed for such associations via linear regressions with adjusting covariates included. Finally, DNAm at PPG-associated CpGs were evaluated for their association with asthma and allergic rhinitis using logistic regressions, adjusting for covariates. The impact of cell heterogeneity on the findings was assessed. Statistical significance was set at <i>p</i> < 0.05.</p><p><strong>Results: </strong>In total, 42 CpGs passed screening, with 41 remaining statistically significant after adjusting for covariates and cell types (<i>p</i> < 0.05). High PPG exposure was associated with lower DNAm at cg12318501 (<i>ZNF99</i>, β = -0.029, <i>p</i> = 0.032) and cg00929606 (<i>ADM2</i>, β = -0.023, <i>p</i> = 0.008), which subsequently was associated with decreased odds of asthma (OR = 0.11, 95% CI 0.02-0.53, <i>p</i> = 0.006; OR = 0.14, 95% CI 0.02-1.00, <i>p</i> = 0.049). For rhinitis, cg15790214 (<i>HCG11</i>) was shown to play such a role as a mediator (β = -0.027, <i>p</i> ≤ 0.0001; OR = 0.22, 95% CI 0.07-0.72, <i>p</i> = 0.01).</p><p><strong>Conclusions: </strong>The association of PPG exposure with childhood asthma and allergic rhinitis incidence is potentially mediated by DNAm at birth.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11940834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143712265","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":"Investigating Single-Molecule Molecular Inversion Probes for Medium-Scale Targeted DNA Methylation Analysis.","authors":"Roy B Simons, Hieab H H Adams, Manfred Kayser, Athina Vidaki","doi":"10.3390/epigenomes9010008","DOIUrl":"10.3390/epigenomes9010008","url":null,"abstract":"<p><strong>Background: </strong>Epigenetic biomarkers, particularly CpG methylation, are increasingly employed in clinical and forensic settings. However, we still lack a cost-effective, sensitive, medium-scale method for the analysis of hundreds to thousands of user-defined CpGs suitable for minute DNA input amounts (<10 ng). In this study, motivated by promising results in the genetics field, we investigated single-molecule molecular inversion probes (smMIPs) for simultaneous analysis of hundreds of CpGs by using an example set of 514 age-associated CpGs (Zhang model).</p><p><strong>Methods: </strong>First, we developed a novel smMIP design tool to suit bisulfite-converted DNA (Locksmith). Then, to optimize the capture process, we performed single-probe capture for ten selected, representative smMIPs. Based on this pilot, the full smMIP panel was tested under varying capture conditions, including hybridization and elongation temperature, smMIP and template DNA amounts, dNTP concentration and elongation time.</p><p><strong>Results: </strong>Overall, we found that the capture efficiency was highly probe-(and hence, sequence-) dependent, with a heterogeneous coverage distribution across CpGs higher than the 1000-fold range. Considering CpGs with at least 20X coverage, we yielded robust methylation detection with levels comparable to those obtained from the gold standard EPIC microarray analysis (Pearsons's r: 0.96).</p><p><strong>Conclusions: </strong>The observed low specificity and uniformity indicate that smMIPs in their current form are not compatible with the lowered complexity of bisulfite-converted DNA.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143712257","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":"Isothiocyanates Enhance the Anti-Melanoma Effect of Zebularine Through Modulation of Apoptosis and Regulation of DNMTs' Expression, Chromatin Configuration and Histone Posttranslational Modifications Associated with Altered Gene Expression Patterns.","authors":"Ioannis Anestopoulos, Ioannis Paraskevaidis, Sotiris Kyriakou, Louiza Potamiti, Dimitrios T Trafalis, Sotiris Botaitis, Rodrigo Franco, Aglaia Pappa, Mihalis I Panayiotidis","doi":"10.3390/epigenomes9010007","DOIUrl":"10.3390/epigenomes9010007","url":null,"abstract":"<p><p><b>Background:</b> In the present study, we aimed to characterize the cytotoxic efficacy of Zebularine either as a single agent or in combination with various isothiocyanates in an in vitro model consisting of human melanoma (A375, Colo-679) as well as non-tumorigenic immortalized keratinocyte (HaCaT) cells. <b>Methods:</b> In this model, we have evaluated the anti-melanoma effect of Zebularine (in single and combinatorial protocols) in terms of cell viability, apoptotic induction and alterations in ultrastructural chromatin configuration, protein expression levels of DNA methyltransferases (DNMTs) and associated histone epigenetic marks capable of mediating gene expression. <b>Results:</b> Exposure to Zebularine resulted in dose- and time-dependent cytotoxicity through apoptotic induction in malignant melanoma cells, while neighboring non-tumorigenic keratinocytes remained unaffected. A more profound response was observed in combinational protocols, as evidenced by a further decline in cell viability leading to an even more robust apoptotic induction followed by a differential response (i.e., activation/de-activation) of various apoptotic genes. Furthermore, combined exposure protocols caused a significant decrease of DNMT1, DNMT3A and DNMT3B protein expression levels together with alterations in ultrastructural chromatin configuration and protein expression levels of specific histone modification marks capable of modulating gene expression. <b>Conclusions:</b> Overall, we have developed a novel experimental approach capable of potentiating the cytotoxic efficacy of Zebularine against human malignant melanoma cells while at the same time maintaining a non-cytotoxic profile against neighboring non-tumorigenic keratinocyte (HaCaT) cells.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143712263","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":"Novel Epigenetics Control (EpC) Nanocarrier for Cancer Therapy Through Dual-Targeting Approach to DNA Methyltransferase and Ten-Eleven Translocation Enzymes.","authors":"Risa Mitsuhashi, Kiyoshi Sato, Hiroyoshi Kawakami","doi":"10.3390/epigenomes9010006","DOIUrl":"10.3390/epigenomes9010006","url":null,"abstract":"<p><strong>Background/objectives: </strong>Aberrant hypermethylation in the promoter regions of tumor suppressor genes facilitates the pathogenesis and progression of cancer. Therefore, inhibitors targeting DNA methyltransferase (DNMT) have been tested in clinical studies. However, the current monotherapy of DNMT inhibitors shows limited efficacy. Furthermore, the mechanism of action of DNMT inhibitors is DNA replication-dependent. To address these limitations, we developed a novel core-shell-type \"epigenetics control (EpC) nanocarrier\" that encapsulated decitabine (5-aza-dC) in the PLGA core nanoparticle and hybridized TET1 gene-encoding pDNA on the lipid shell surface. This study aimed to evaluate whether the dual delivery of DNMT inhibitors and pDNA of TET1 could synergistically enhance tumor suppressor gene expression and induce cell cycle arrest and/or apoptosis in cancer cells. Herein, we demonstrate the potential of the EpC carrier in HCT116 human colon cancer cells to upregulate tumor suppressor gene expression and rapidly achieve cell cycle arrest.</p><p><strong>Methods: </strong>PLGA core nanoparticles were prepared by the W/O/W double emulsion method. The formation of core-shell nanoparticles and complexation with pDNA were investigated and optimized by dynamic light scattering, zeta potential measurement, and agarose gel electrophoresis. The cellular uptake and transfection efficiency were measured by confocal laser scanning microscopy and a luciferase assay, respectively. The expression of p53 protein was detected by Western blotting. The anti-tumor effects of the EpC nanocarrier were evaluated by cell cycle analysis and an apoptosis assay.</p><p><strong>Results: </strong>The EpC nanocarrier delivered the DNMT inhibitor and TET gene-encoding pDNA into HCT116 cells. It promoted the expression of the tumor suppressor protein p53 and induced rapid cell cycle arrest in the G2/M phase in HCT116 cells.</p><p><strong>Conclusions: </strong>Our findings suggest that the dual-targeting of DNMT and TET enzymes effectively repairs aberrant DNA methylation and induces growth arrest in cancer cells, and the dual-targeting strategy may contribute to the advancement of epigenetic cancer therapy.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469946","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":"Epigenomic Echoes-Decoding Genomic and Epigenetic Instability to Distinguish Lung Cancer Types and Predict Relapse.","authors":"Alexandra A Baumann, Zholdas Buribayev, Olaf Wolkenhauer, Amankeldi A Salybekov, Markus Wolfien","doi":"10.3390/epigenomes9010005","DOIUrl":"10.3390/epigenomes9010005","url":null,"abstract":"<p><p>Genomic and epigenomic instability are defining features of cancer, driving tumor progression, heterogeneity, and therapeutic resistance. Central to this process are epigenetic echoes, persistent and dynamic modifications in DNA methylation, histone modifications, non-coding RNA regulation, and chromatin remodeling that mirror underlying genomic chaos and actively influence cancer cell behavior. This review delves into the complex relationship between genomic instability and these epigenetic echoes, illustrating how they collectively shape the cancer genome, affect DNA repair mechanisms, and contribute to tumor evolution. However, the dynamic, context-dependent nature of epigenetic changes presents scientific and ethical challenges, particularly concerning privacy and clinical applicability. Focusing on lung cancer, we examine how specific epigenetic patterns function as biomarkers for distinguishing cancer subtypes and monitoring disease progression and relapse.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469911","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":"Single-Molecule Nanopore Sequencing of the CpG Island from the Promoter of O6-Methylguanine-DNA Methyltransferase Provides Insights into the Mechanism of De Novo Methylation of G/C-Rich Regions.","authors":"Alexander V Sergeev, Daniil P Malyshev, Adelya I Genatullina, Galina V Pavlova, Elizaveta S Gromova, Maria I Zvereva","doi":"10.3390/epigenomes9010004","DOIUrl":"10.3390/epigenomes9010004","url":null,"abstract":"<p><strong>Background: </strong>The methylation of cytosine residues at CpG sites within the O6-methylguanine-DNA methyltransferase (<i>MGMT</i>) promoter is a key biomarker in glioblastoma therapy. The <i>MGMT</i> promoter (MGMTp) contains multiple guanine-rich sequences capable of folding into G-quadruplexes (G4s), but their relevance for MGMTp methylation is poorly understood.</p><p><strong>Objectives: </strong>Our study explores the impact of potential G-quadruplex-forming sequences (PQS) in the <i>MGMT</i> promoter CpG island on the activity of de novo DNA methyltransferase Dnmt3a. Additionally, we investigate their influence on the accuracy of methylation pattern detection using nanopore sequencing.</p><p><strong>Methods: </strong>Nanopore sequencing was employed to analyze the methylation of 94 clinically significant CpG sites in the human MGMTp using an in vitro de novo methylation system. Circular dichroism spectroscopy was used to identify G4 structures within the MGMTp CpG island. Interactions between the catalytic domain of Dnmt3a and the PQS from the MGMTp were examined by biolayer interferometry.</p><p><strong>Results: </strong>Guanine-rich DNA strands of the PQSs in the MGMTp were hypomethylated, while the complementary cytosine-rich strands were methylated by DNA methyltransferase Dnmt3a with higher efficiency. The accuracy of detecting modified bases in the PQS was significantly lower compared to surrounding sequences. Single-stranded guanine-rich DNA sequences from the MGMTp exhibited strong binding to Dnmt3a-CD, with an affinity approximately 10 times higher than their cytosine-rich complements (<i>K</i>_d = 3 × 10^-8 M and 3 × 10^-7 M, respectively). By binding to Dnmt3a, G4-forming oligonucleotides from MGMTp effectively inhibited the methylation reaction (IC₅₀ 6 × 10^-7 M).</p><p><strong>Conclusions: </strong>The obtained data indicate the role of PQSs in establishing de novo methylation of the <i>MGMT</i> promoter. They also highlight the challenges of sequencing guanine-rich regions and the impact of specific de novo methylation patterns on clinical data interpretation.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469864","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":"Epigenetics in Skin Homeostasis and Ageing.","authors":"Iasonas Dermitzakis, Stella Aikaterini Kyriakoudi, Sofia Chatzianagnosti, Despoina Chatzi, Efstratios Vakirlis, Soultana Meditskou, Maria Eleni Manthou, Paschalis Theotokis","doi":"10.3390/epigenomes9010003","DOIUrl":"10.3390/epigenomes9010003","url":null,"abstract":"<p><p>The skin, the largest organ of the human body, plays numerous essential roles, including protection against environmental hazards and the regulation of body temperature. The processes of skin homeostasis and ageing are complex and influenced by many factors, with epigenetic mechanisms being particularly significant. Epigenetics refers to the regulation of gene expression without altering the underlying DNA sequence. The dynamic nature of the skin, characterized by constant cellular turnover and responsiveness to environmental stimuli, requires precise gene activity control. This control is largely mediated by epigenetic modifications such as DNA methylation, histone modification, and regulation by non-coding RNAs. The present review endeavours to provide a comprehensive exploration and elucidation of the role of epigenetic mechanisms in regulating skin homeostasis and ageing. By integrating our current knowledge of epigenetic modifications with the latest advancements in dermatological research, we can gain a deeper comprehension of the complex regulatory networks that govern skin biology. Understanding these mechanisms also presents promising avenues for therapeutic interventions aimed at improving skin health and mitigating age-related skin conditions.</p>","PeriodicalId":55768,"journal":{"name":"Epigenomes","volume":"9 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025680","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}