Epigenetics最新文献

{"title":"Chromatin accessibility profiling of Treg cells in acute urticaria.","authors":"Leilei Wen, Xiaojing Zhang, Qiaoshan Yang, Fusheng Zhou","doi":"10.1080/15592294.2025.2503126","DOIUrl":"10.1080/15592294.2025.2503126","url":null,"abstract":"<p><p>Acute urticaria can be a presenting symptom of anaphylaxis characterized by transient red swellings or fulminant wheals, often accompanied by severe pruritus. Numerous studies have substantiated the important involvement of regulatory T cells (Tregs) in the occurrence of allergic diseases and autoimmune diseases. However, the role of Tregs in the pathogenesis of acute urticaria is unclear. In this study, we found that the frequency of Tregs in peripheral blood mononuclear cells (PBMCs) was decreased in patients with acute urticaria compared with normal controls by flow cytometry. Analysis of Assay for transposase-accessible chromatin with sequencing (ATAC-seq) data identified 28 differentially accessible regions comparing Tregs from healthy individuals and patients with acute urticaria, all showing increased chromatin accessibility in the Tregs from acute urticaria. IL-1b was highly expressed in sera of patients with acute urticaria and the level of IL-1b was moderately positively related to white blood cell count. The elevated expression of IL-1b may be due to the diminished immune-suppressive function following the decline of Tregs in this study. We found that <i>IL1B</i> gene expression was also significantly increased in the skin lesions of both chronic spontaneous urticaria and solar urticaria compared to healthy controls. IL1B might play a key role in the development of acute urticaria and IL1B could be a potential prognostic biomarker and therapeutic target in urticaria.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2503126"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12077484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucocorticoid receptor epigenetic activity in the heart.","authors":"Olukunle Akinborewa, Mattia Quattrocelli","doi":"10.1080/15592294.2025.2468113","DOIUrl":"10.1080/15592294.2025.2468113","url":null,"abstract":"<p><p>The glucocorticoid receptor (GR) is a critical nuclear receptor that regulates gene expression in diverse tissues, including the heart, where it plays a key role in maintaining cardiovascular health. GR signaling influences essential processes within cardiomyocytes, including hypertrophy, calcium handling, and metabolic balance, all of which are vital for proper cardiac function. Dysregulation of GR activity has been implicated in various cardiovascular diseases (CVDs), highlighting the potential of GR as a therapeutic target. Remarkably, recent insights into GR's epigenetic regulation and its interaction with circadian rhythms reveal opportunities to optimize therapeutic strategies by aligning glucocorticoid administration with circadian timing. In this review, we provide an overview of the glucocorticoid receptor's role in cardiac physiology, detailing its genomic and non-genomic pathways, interactions with epigenetic and circadian regulatory mechanisms, and implications for cardiovascular disease. By dissecting these molecular interactions, this review outlines the potential of epigenetically informed and circadian-timed interventions that could change the current paradigms of CVD treatments in favor of precise and effective therapies.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2468113"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11866966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143499980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA-based cell typing in menstrual effluent identifies cell type variation by sample collection method: toward noninvasive biomarker development for women's health.","authors":"Irma M Vlasac, Hannah G Stolrow, Zaneta M Thayer, Brock C Christensen, Luisa Rivera","doi":"10.1080/15592294.2025.2453275","DOIUrl":"10.1080/15592294.2025.2453275","url":null,"abstract":"<p><p>Menstrual effluent cell profiles have potential as noninvasive biomarkers of female reproductive and gynecological health and disease. We used DNA methylation-based cell type deconvolution (methylation cytometry) to identify cell type profiles in self-collected menstrual effluent. During the second day of their menstrual cycle, healthy participants collected menstrual effluent using a vaginal swab, menstrual cup, and pad. Immune cell proportions were highest in menstrual cup samples, and epithelial cells were highest in swab samples. Our work demonstrates the feasibility and utility of menstrual effluent cell profiling in population-level research using remotely collected samples and DNA methylation.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2453275"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12698062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anesthetic-induced epigenetic alterations: mechanisms and long-term clinical implications.","authors":"Elham Shahidi Delshad, Afzal Shamsi, Mahdieh Mehrab Mohseni, Niloofar Abak, Mostafa Saberian","doi":"10.1080/15592294.2025.2599650","DOIUrl":"10.1080/15592294.2025.2599650","url":null,"abstract":"<p><p>This review explores how anesthetic agents influence epigenetic mechanisms such as DNA methylation, histone modifications, and non-coding RNA expression, and their lasting clinical effects. Common anesthetics, including propofol, isoflurane, sevoflurane, and local or regional agents, trigger epigenetic alterations. Preclinical research, especially in developing and aging brains, ties these changes to neurodevelopmental delays, cognitive decline, and shifts in immune and metabolic processes. While clinical studies are ongoing, accumulating evidence reveals that anesthesia triggers both transient and persistent epigenetic modifications, with potential links to postoperative cognitive dysfunction, prolonged inflammation, and altered developmental trajectories. Pediatric and elderly patients show heightened susceptibility due to brain plasticity or diminished resilience. Leveraging epigenetic knowledge could pave the way for tailored anesthesia approaches, reducing long-term risks. Moreover, emerging evidence suggests intergenerational transmission of these epigenetic changes via germline reprogramming, potentially affecting neurodevelopment and disease susceptibility in offspring. Future studies should prioritize large-scale human trials, detailed mechanistic insights, and identification of epigenetic biomarkers to guide safer anesthetic development. This review highlights anesthesia's broader systemic consequences, extending beyond immediate cognitive impacts, and underscores its relevance to personalized medicine.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2599650"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12688258/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145707527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Strength of evidence for paternal influence on offspring epigenome in observational human studies: a systematic review and risk-of-bias appraisal for non-randomized exposures.","authors":"Ka Kei Sum, Mark A Burton, Cristina Garcia-Maurino Alcazar, Ai Ling Teh, Keith M Godfrey, Jonathan Yinhao Huang","doi":"10.1080/15592294.2025.2594322","DOIUrl":"10.1080/15592294.2025.2594322","url":null,"abstract":"<p><p>Paternal influence on the offspring epigenome is difficult to interpret in observational human studies due to heterogeneous designs, causing varying susceptibility to bias and non-causal explanations. We conducted a systematic review (CRD42022302695) of paternal exposures before or during pregnancy in relation to the offspring epigenome, focusing on characteristics affecting causal interpretation and reproducibility. We searched three electronic databases for human studies published between 2003 and 2023. Eligible studies assessed paternal factors before or during pregnancy as exposures, and epigenetic mechanisms as outcomes. Risk of bias (RoB) was evaluated using ROBINS-E. The most frequently studied paternal factors were BMI/obesity (7), age (7), smoking (5), and socioeconomic status (SES) (4). All 28 studies assessed DNA methylation; two additionally explored miRNA expression. Most studies were rated 'high' or 'very high' RoB, primarily due to unclear exposure measurement and confounding. Findings showed limited overlap in CpG sites and genomic regions across studies. However, exposures that were stable (<i>e.g</i>. SES) or had clearly defined timing produced more consistent results. Notably, studies with clearly defined timing of paternal smoking suggested preconception exposure may influence offspring epigenetic pathways related to innate immunity but not pregnancy exposure. In contrast, paternal factors with poorly defined experimental analogues, such as BMI, provided inconsistent results. Aligning study design more closely with clinical trials or animal models, by clearly defining populations and exposures, may result in more reliable and replicable findings. Frameworks like 'target trial emulation,' offer a promising approach to improve reproducibility and interpretability of future research on paternal effects on offspring epigenome.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2594322"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145713709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress on the mechanism of tumor cell ferroptosis regulation by epigenetics.","authors":"Yuyang Xiao, Mengyang He, Xupeng Zhang, Meng Yang, Zhangchi Yuan, Shanhu Yao, Yuexiang Qin","doi":"10.1080/15592294.2025.2500949","DOIUrl":"https://doi.org/10.1080/15592294.2025.2500949","url":null,"abstract":"<p><p>Cancer remains a significant barrier to human longevity and a leading cause of mortality worldwide. Despite advancements in cancer therapies, challenges such as cellular toxicity and drug resistance to chemotherapy persist. Regulated cell death (RCD), once regarded as a passive process, is now recognized as a programmed mechanism with distinct biochemical and morphological characteristics, thereby presenting new therapeutic opportunities. Ferroptosis, a novel form of RCD characterized by iron-dependent lipid peroxidation and unique mitochondrial damage, differs from apoptosis, autophagy, and necroptosis. It is driven by reactive oxygen species (ROS)-induced lipid peroxidation and is implicated in tumorigenesis, anti-tumor immunity, and resistance, particularly in tumors undergoing epithelial-mesenchymal transition. Moreover, ferroptosis is associated with ischemic organ damage, degenerative diseases, and aging, regulated by various cellular metabolic processes, including redox balance, iron metabolism, and amino acid, lipid, and glucose metabolism. This review focuses on the role of epigenetic factors in tumor ferroptosis, exploring their mechanisms and potential applications in cancer therapy. It synthesizes current knowledge to provide a comprehensive understanding of epigenetic regulation in tumor cell ferroptosis, offering insights for future research and clinical applications.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2500949"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12064064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel lncRNA, Lnc21q22.11, suppresses gastric cancer growth by inhibiting MEK/ERK pathway.","authors":"Cheng Zhu, Meiying Zhang, Weili Yang, Aiai Gao, Xiaoyuan Yu, Xiaomo Su, Runsheng Chen, Mingzhou Guo","doi":"10.1080/15592294.2025.2512764","DOIUrl":"10.1080/15592294.2025.2512764","url":null,"abstract":"<p><p>Gastric cancer (GC) is one of the most common malignancies with limited treatment options and poor prognosis. Therefore, it is necessary to identify new markers for the development of novel therapeutic strategies. Long non-coding RNAs (lncRNAs) have emerged as pivotal players in cancer. However, RNA-based cancer therapy has been challenged by non-specificity and adverse immune effects. Thus, a comprehensive understanding of the functional roles of lncRNAs and their regulatory networks in downstream pathways may provide more specific targets. In this study, we identified a novel lncRNA, Lnc21q22.11, encoded by the region of chromosome 21q22.11. The full-length transcript was 1202 nt, and its expression was reduced in GC. The expression of Lnc21q22.11 was regulated by histone methylation. Lnc21q22.11 inhibited GC cell proliferation, colony formation, invasion, and migration. Lnc21q22.11 suppressed N87 cell xenograft growth in mice. Mechanistically, Lnc21q22.11 inhibited the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) signaling pathway by interacting with MYH9 in GC cells. Loss of or reduced Lnc21q22.11 expression sensitized GC cells to MEK inhibitor. In conclusion, Lnc21q22.11 is a novel lncRNA in gastric cancer. It suppresses gastric cancer growth by inhibiting the MEK/ERK signaling pathway both <i>in vitro</i> and <i>in vivo</i>.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2512764"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential methylation in blood pressure control genes is associated to essential hypertension in African Brazilian populations.","authors":"Camila Cristina Avila Martins, Mariana Maschietto, Lilian Kimura, Lucas Alvizi, Kelly Nunes, Vinícius Magalhães Borges, Ana Cristina Victorino Krepischi, Regina Célia Mingroni-Netto","doi":"10.1080/15592294.2025.2477850","DOIUrl":"10.1080/15592294.2025.2477850","url":null,"abstract":"<p><p>While genetic studies have provided insights into essential hypertension (EH, defined by high blood pressure ≥140/90 mmHg), investigation through epigenetics may address gaps in understanding its heritability. This study focused on African Brazilian populations in Vale do Ribeira River region, due to their high hypertension prevalence. We aimed to determine if DNA methylation is linked to hypertension susceptibility, through a genome-wide evaluation of 80 peripheral blood samples from normotensive (39) and hypertensive (41) individuals, with Infinium Methylation EPIC BeadChip platform. Data were analyzed using ChAMP package and cross-referenced with information from databases such as EWAS Atlas, GWAS catalog, GeneCards, literature, and tools such as VarElect and EWAS Toolkit. The comparison between hypertensive and normotensive revealed 190 differentially methylated CpG positions (DMPs) and 46 differentially methylated regions (DMRs), both with <i>p</i>-value ≤0.05. Among the DMPs, 27 were found to have a plausible role in blood pressure. Among the DMRs, those mapped to <i>ABAT, BLCAP, CERS3, EIF4E, FMN1, GABBR1, HLA-DQB2, HOXA5, IL5RA, KCNH2, MIR487B, MIR539, MIR886, MKRN3, NUDT12, PON3, RNF39, RWDD3,</i> and <i>TSHBS1</i> were highlighted because of their lowest <i>p</i>-values, current literature, and/or VarElect prioritization. Our findings suggest that differences in methylation contribute to the high susceptibility to essential hypertension in these populations.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2477850"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between skeletal muscle and the brain during physical activity - in search of epigenetic mechanisms.","authors":"Cayla Boycott, Ewa Kilanczyk, Huiying A Zhang, Jiaxi Zhang, Arian Abolhassani, Malgorzata Kubiak, Jan Celichowski, Katarzyna Kryściak, Dominika Gruszka, Joanna H Sliwowska, Barbara Stefanska","doi":"10.1080/15592294.2025.2590237","DOIUrl":"10.1080/15592294.2025.2590237","url":null,"abstract":"<p><p>Recent research highlights the crucial role of muscle-brain crosstalk in metabolic regulation, particularly in individuals with type 2 diabetes and obesity. Myokines, protein hormones secreted by skeletal muscle, play a crucial role in this communication, influencing brain functions such as neuroplasticity, memory, and mood. Specific myokines like cathepsin B, FNDC5/irisin and interleukin-6 have been identified as key players in this muscle-brain axis. Physical activity modulates the production of these molecular factors, enhancing muscle-brain crosstalk and influencing cellular interactions. Moreover, exercise training may lead to adaptive long-term changes in gene expression, mediated by epigenetic regulators. Metabolic pathways activated during exercise can directly impact epigenetic marks by modulating the availability of metabolic intermediates required for these modifications. In the present review, we summarize the latest findings on the association between obesity/diabetes and cognitive impairment due to hippocampal dysfunction, and elaborate on how exercise influences cognitive functions via the communication between skeletal muscle and the brain. We focus on the underlying mechanisms responsible for the muscle-brain crosstalk, emphasizing dynamic changes in the epigenome and epitranscriptome, which sheds light on novel preventive and therapeutic approaches to combat obesity and cognitive decline.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2590237"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12645880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145586336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adaptation and changing phenotypes through transgenerational epigenetics.","authors":"Lon J Van Winkle, Rebecca J Ryznar, Philip M Iannaccone","doi":"10.1080/15592294.2025.2460246","DOIUrl":"10.1080/15592294.2025.2460246","url":null,"abstract":"<p><p>In this article collection, we describe how noncoding epigenetic changes in DNA are transmitted across multiple generations in eukaryotic organisms including plants and animals. And such environmentally induced biochemical alterations of DNA and histones result in profound changes in gene expression. In plants and invertebrate animals, transgenerational epigenetic inheritance has been well documented, and it continues to be substantiated in humans and other vertebrates. These exciting new discoveries have profound consequences for changing as well as maintaining phenotypes expressed by various life forms and, thus, the changes likely contribute to evolution. And in a more practical way, such studies are very important because of the likely transgenerational inheritance of diseases and disorders, such as type 2 diabetes mellitus and obesity.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2460246"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144834434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}