Epigenomics最新文献_第2页

Longitudinal study of genome-wide DNA methylation in individuals with and without post-acute symptoms following SARS-CoV-2 infection. 在有和没有SARS-CoV-2感染后急性后症状的个体中全基因组DNA甲基化的纵向研究

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-04-10 DOI: 10.1080/17501911.2026.2656361

Jon Bohlin, Yunsung Lee, Ida Henriette Caspersen, Anna Hayman Robertson, Christian M Page, Håkon K Gjessing, Astanand Jugessur, Per Magnus, Siri Mjaaland, Lill Trogstad

{"title":"Longitudinal study of genome-wide DNA methylation in individuals with and without post-acute symptoms following SARS-CoV-2 infection.","authors":"Jon Bohlin, Yunsung Lee, Ida Henriette Caspersen, Anna Hayman Robertson, Christian M Page, Håkon K Gjessing, Astanand Jugessur, Per Magnus, Siri Mjaaland, Lill Trogstad","doi":"10.1080/17501911.2026.2656361","DOIUrl":"10.1080/17501911.2026.2656361","url":null,"abstract":"Background: Symptoms following SARS-CoV-2 infection, referred to as Long-COVID, have been reported since the pandemic. We investigated whether COVID-19 or Long-COVID is associated with persistent genome-wide DNA methylation (DNAm) changes in whole blood using a longitudinal design.Methods: DNAm was measured using the Illumina EPIC V2 platform (859,651 CpGs) in 297 adult participants (594 samples in total) from two Norwegian population-based cohorts, with samples collected pre-infection (2020) and during the pandemic (2023). Participants were classified as Long-COVID, COVID-19 (no persistent symptoms), or not infected.Results: No significant DNAm differences were observed between Long-COVID and not infected at either time point (p = 0.745(FDR)) or during the pandemic specifically (p = 0.629(FDR)). Likewise, no differences were detected between COVID-19 and not infected across both time points (p = 0.883(FDR)) or during the pandemic (p = 0.287(FDR)). Sex-stratified analyses of the X chromosome revealed no significant DNAm differences for Long-COVID or COVID-19 in males (both p = 0.999(FDR)) or females (both p = 0.999(FDR)). Epigenetic age acceleration was also evaluated using DunedinPACE (DP) and PhenoAge (PA), but no significant differences were detected for Long-COVID (p = 0.695 [DP], p = 0.528 [PA]) or COVID-19 (p = 0.624 [DP], p = 0.348 [PA]).Conclusion: No persistent epigenetic age- or DNAm based differences due to Long-COVID or SARS-CoV-2 infection were detected in our cohorts.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"411-419"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Computational-based integrative methylome-transcriptome analysis reveals widespread enhancer hypomethylation in esophageal carcinoma. 基于计算的综合甲基组-转录组分析揭示了食管癌中广泛存在的增强子低甲基化。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-04-14 DOI: 10.1080/17501911.2026.2654596

Akbar Ali, Tengku Ahmad Damitri Al Astani Tengku Din, Muhammad Irfan Abdul Jalal, Wan Nor Arifin, Mai Abdel Haleem A Abusalah, Alqassem Hamdallah Abuarqoub, Naveed Ahmed

{"title":"Computational-based integrative methylome-transcriptome analysis reveals widespread enhancer hypomethylation in esophageal carcinoma.","authors":"Akbar Ali, Tengku Ahmad Damitri Al Astani Tengku Din, Muhammad Irfan Abdul Jalal, Wan Nor Arifin, Mai Abdel Haleem A Abusalah, Alqassem Hamdallah Abuarqoub, Naveed Ahmed","doi":"10.1080/17501911.2026.2654596","DOIUrl":"10.1080/17501911.2026.2654596","url":null,"abstract":"Background: Esophageal carcinoma (ESCA), comprising esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), has a poor prognosis due to late diagnosis and incomplete molecular characterization. We sought to define the ESCA epigenomic landscape by integrating methylome and transcriptome data across both subtypes.Research design and methods: TCGA-ESCA HumanMethylation450K and RNA-seq profiles (182 tumors: 95 ESCC and 87 EAC; 64 normal tissues) were analyzed using ELMER and Bioconductor workflows. Differentially methylated probes were annotated by genomic category, probe-gene coupling was tested by Spearman correlation, and a LASSO-penalized 12-CpG classifier was trained and externally validated in an independent GEO cohort (GSE68303; n = 43).Results: ESCA showed pervasive enhancer hypomethylation, with 72.5% of the hypomethylated probes mapping to the distal enhancers. Methylation-expression coupling identified LINC02547 and PYGL as candidate effector genes, and enriched transcription factor motifs included AP-1 and NFIL3. The classifier achieved a cross-validated AUC of 0.996, approximately 0.99, sensitivity at 95% specificity, and reproducible performance across ESCC and EAC subtypes. Advanced disease stage was the dominant prognostic factor in multivariable survival models.Conclusions: Enhancer hypomethylation is a hallmark of ESCA, nominating LINC02547 and PYGL as biomarker candidates with diagnostic/prognostic promise. Limitations include retrospective design and need for experimental validation.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"397-410"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

KMT2B induces the H3K4 trimethylation of RBBP6 promoter to enhance the ¹³¹I sensitivity in thyroid carcinoma by restraining STAT1/DPP4 axis. KMT2B诱导RBBP6启动子H3K4三甲基化，通过抑制STAT1/DPP4轴增强甲状腺癌中131I的敏感性。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-04-21 DOI: 10.1080/17501911.2026.2658070

Meiqun Wang, Zhi Wang, Haifeng Yang, Tao Zhou

{"title":"KMT2B induces the H3K4 trimethylation of RBBP6 promoter to enhance the 131I sensitivity in thyroid carcinoma by restraining STAT1/DPP4 axis.","authors":"Meiqun Wang, Zhi Wang, Haifeng Yang, Tao Zhou","doi":"10.1080/17501911.2026.2658070","DOIUrl":"10.1080/17501911.2026.2658070","url":null,"abstract":"Background: Radioactive iodine (RAI) resistance severely limits treatment efficacy in thyroid carcinoma (THCA), yet its molecular underpinnings remain incompletely elucidated. In the present study, we sought to reveal the molecular mechanism by which histone lysine methyltransferase 2B (KMT2B) regulated dipeptidyl peptidase 4 (DPP4)-mediated THCA resistance to RAI.Methods: Sequential Chromatin immunoprecipitation (ChIP)-re-ChIP assay was performed to evaluate the co-binding of KMT2B and H3K4 trimethylation (H3K4me3) at the retinoblastoma-binding protein 6 (RBBP6) promoter. Co-immunoprecipitation analyzed the STAT1 ubiquitination levels. Co-immunoprecipitation and GST pull-down analyzed the protein-protein interaction between RBBP6 and STAT1. STAT1 and DPP4 promoter binding were assessed via a ChIP assay.Results: DPP4 was upregulated in 131I-resistant THCA cells. The knockdown of DPP4 inhibited the THCA cell resistance to RAI. STAT1 bound to the DPP4 promoter to enhance its transcription. RBBP6 facilitated the ubiquitinated degradation of STAT1 protein. Overexpression of DPP4 abrogated the THCA tumor-suppressive effects mediated by RBBP6 overexpression. KMT2B augmented the expression of RBBP6 through H3K4me3 modification. The inhibitory effects of KMT2B overexpression on proliferation, migration, and invasion of 131I-resistant THCA cells were counteracted by DPP4 overexpression.Conclusion: KMT2B enhanced RAI sensitivity in THCA via H3K4me3-mediated RBBP6 upregulation, driving STAT1 ubiquitination and degradation to suppress DPP4 transcription.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"421-436"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Estrogen-induced epigenetic silencing of myotrophin reduces proliferation and is associated with chemosensitivity in hepatocellular carcinoma cells. 雌激素诱导的肌营养蛋白的表观遗传沉默减少了肝癌细胞的增殖，并与化疗敏感性有关。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-04-08 DOI: 10.1080/17501911.2026.2654575

Jibran Sualeh Muhammad, Bilal Rah, Nouf Khan, Aisha Janeeh, Jasmin Shafarin, Iman Talaat, Kirsten C Sadler, Mawieh Hamad

{"title":"Estrogen-induced epigenetic silencing of myotrophin reduces proliferation and is associated with chemosensitivity in hepatocellular carcinoma cells.","authors":"Jibran Sualeh Muhammad, Bilal Rah, Nouf Khan, Aisha Janeeh, Jasmin Shafarin, Iman Talaat, Kirsten C Sadler, Mawieh Hamad","doi":"10.1080/17501911.2026.2654575","DOIUrl":"10.1080/17501911.2026.2654575","url":null,"abstract":"Background: Hepatocellular carcinoma (HCC) carries poor survival and limited response to conventional chemotherapy. Epidemiological evidence suggests a lower incidence of HCC in females, implicating estrogen (E2) in tumor suppression. The epigenetic mechanisms underlying estrogen-associated protection remain incompletely defined.Research design and methods: We investigated the relationship between E2 exposure, myotrophin (MTPN) expression, and chemotherapy response using TCGA HCC datasets, human hepatoma cell lines (HepG2, HUH7), zebrafish larvae, and a diethylnitrosamine (DEN)-induced mouse model. Cells were pretreated with E2 (10 nM, 6 h) followed by doxorubicin (DOX; up to 2.0 nM, 24 h). Promoter methylation was assessed by quantitative methylation-specific PCR. Cell viability, apoptosis, DNA damage, liver size, tumor burden, and protein expression were evaluated.Results: MTPN was overexpressed and hypomethylated in human HCC. E2 exposure reduced MTPN expression and increased promoter methylation in vitro and in vivo. MTPN knockdown decreased HCC cell viability and proliferation. E2 pretreatment enhanced DOX-associated apoptotic responses in hepatoma cells. In DEN-induced HCC, E2 reduced liver size, tumor burden, and hepatic MTPN protein levels.Conclusions: Estrogen-associated epigenetic repression of MTPN contributes to growth suppression in HCC and is associated with enhanced cytotoxic responses to DOX. Clinical validation is required to determine prognostic or therapeutic relevance.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"385-396"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-coding RNAs regulation in breast cancer pathogenesis. 非编码rna调控乳腺癌发病机制。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-03-10 DOI: 10.1080/17501911.2026.2642583

Bala Gur Dedeoglu, Senem Noyan, Kübra Nur Kaplan İlhan

{"title":"Non-coding RNAs regulation in breast cancer pathogenesis.","authors":"Bala Gur Dedeoglu, Senem Noyan, Kübra Nur Kaplan İlhan","doi":"10.1080/17501911.2026.2642583","DOIUrl":"10.1080/17501911.2026.2642583","url":null,"abstract":"Breast cancer represents a molecularly heterogeneous disease shaped by complex genetic, epigenetic, and transcriptional dysregulation. Non-coding RNAs (ncRNAs) including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) as well as small nucleolar RNAs (snoRNAs), piwi-interacting RNAs (piRNAs), and small nuclear RNAs (snRNAs), have emerged as key epigenetic regulators that integrate multiple layers of gene control. Through interactions with chromatin-modifying enzymes, RNA-binding proteins, and signaling effectors, ncRNAs modulate transcriptional activity, chromatin accessibility, and post-transcriptional stability of target genes. miRNAs predominantly act as post-transcriptional repressors, whereas lncRNAs and circRNAs exert transcriptional and epigenetic control via scaffolding, miRNA sponging, and chromatin remodeling; some circRNAs even encode functional peptides. Aberrant ncRNA expression contributes to proliferation, metastasis, metabolic reprogramming, immune evasion, and therapeutic resistance, with distinct expression signatures associated with triple-negative, HER2-positive, and hormone receptor - positive breast cancers. Owing to their stability and detectability in plasma and exosomes, ncRNAs hold promise as minimally invasive biomarkers for early detection and disease monitoring. Moreover, therapeutic strategies targeting ncRNAs, such as antisense oligonucleotides, RNA interference, CRISPR/Cas-based editing, and ncRNA-derived vaccines, are advancing toward clinical translation. Collectively, ncRNAs redefine the epigenetic landscape of breast cancer, offering a framework for integrated diagnostic and therapeutic approaches in precision oncology.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"493-512"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DNA methyltransferase inhibitors in oncology: clinical progress, limitations and future directions. 肿瘤DNA甲基转移酶抑制剂：临床进展、局限性和未来方向。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-02-28 DOI: 10.1080/17501911.2026.2637418

David C Michael, Parinaz Mehdipour

{"title":"DNA methyltransferase inhibitors in oncology: clinical progress, limitations and future directions.","authors":"David C Michael, Parinaz Mehdipour","doi":"10.1080/17501911.2026.2637418","DOIUrl":"10.1080/17501911.2026.2637418","url":null,"abstract":"Over the past century, cancer therapy has evolved from broadly cytotoxic approaches to mechanism-based treatments. Recognition of epigenetic dysregulation as a cancer hallmark paved the way for epigenetic therapies. The earliest to gain U.S. Food and Drug Administration (FDA) approval were DNA methyltransferase inhibitors (DNMTis), such as azacitidine and decitabine, which remain cornerstone agents in epigenetic therapy. By reversing aberrant DNA hypermethylation, DNMTis restore silenced tumor suppressor pathways, induce cellular differentiation, trigger DNA-damage-driven apoptosis, and enhance tumor immunogenicity. Although DNMTi monotherapy shows limited efficacy particularly in solid tumors, DNMTis can potentiate immunotherapy, chemotherapy or targeted agents in optimized combinatorial modalities to produce antitumor responses and overcome therapeutic resistance. For instance, combining DNMTis with the BCL-2 inhibitor venetoclax has produced substantial clinical benefit in hematologic malignancies and is now an FDA-approved standard-of-care regimen. Emerging dual-epigenetic strategies, including DNMTi and histone deacetylase inhibitors (HDACi), further expand therapeutic potential particularly in hormone-negative cancers. A deeper mechanistic understanding of standard DNMTis, together with further refinement of next-generation DNMTis beyond pharmacokinetic improvements, is essential to achieve more durable anti-cancer responses. Future efforts should prioritize optimized dosing and combinatorial regimens, alongside biomarker-guided patient selection and more targeted epigenetic approaches to improve efficacy, especially in solid tumors.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"463-491"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rewiring the cardiovascular epigenome: the multi-target strategy of traditional Chinese medicine. 心血管表观基因组重组：中医多靶点策略。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-04-01 Epub Date: 2026-03-29 DOI: 10.1080/17501911.2026.2652278

Yuxin Wei, Ruitong Du, Huiyue Yuan, Lihong Wu, Deqiang Yang, Fanjia Meng, Haixue Kuang, Zhibin Wang

{"title":"Rewiring the cardiovascular epigenome: the multi-target strategy of traditional Chinese medicine.","authors":"Yuxin Wei, Ruitong Du, Huiyue Yuan, Lihong Wu, Deqiang Yang, Fanjia Meng, Haixue Kuang, Zhibin Wang","doi":"10.1080/17501911.2026.2652278","DOIUrl":"10.1080/17501911.2026.2652278","url":null,"abstract":"Epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs (ncRNAs), are fundamentally involved in the initiation and progression of cardiovascular diseases (CVDs). An increasing body of evidence suggests that Traditional Chinese Medicines (TCMs), characterized by multi‑component and multi‑target actions, significantly regulate these epigenetic processes. This review summarizes current advances in TCM‑mediated epigenetic regulation in CVDs and outlines how representative herbs, bioactive compounds, and classical formulations are involved in regulating key epigenetic enzymes, chromatin states, and regulatory RNA networks. Mechanistic evidence across three major epigenetic layers is critically evaluated, and emerging technologies, such as multi-omics profiling, single-cell epigenomics, and CRISPR-based epigenome editing, that have facilitated mechanistic elucidation are summarized. Current limitations, including heterogeneous study designs, insufficient mechanistic validation, and the scarcity of high-quality clinical trials, are discussed in depth. The prospects of integrating TCM with precision epigenetic medicine are further discussed, particularly through biomarker-guided interventions and synergistic combinations with modern therapeutics. A clearer mechanistic framework and standardized methodologies will be required to translate TCM-based epigenetic modulation into clinically actionable strategies for the prevention and treatment of CVDs.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"513-529"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Emerging roles of epigenetics in the pathogenesis of sarcopenia. 表观遗传学在肌肉减少症发病机制中的新作用。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-03-01 Epub Date: 2026-03-05 DOI: 10.1080/17501911.2026.2637968

Mei Wu, Yuan Zhao, Shiyan Gu, Han Lu, Yaolei Cha, Yilin Yang, Qing Yang, Lijie Yang, Zhexi Xiao

{"title":"Emerging roles of epigenetics in the pathogenesis of sarcopenia.","authors":"Mei Wu, Yuan Zhao, Shiyan Gu, Han Lu, Yaolei Cha, Yilin Yang, Qing Yang, Lijie Yang, Zhexi Xiao","doi":"10.1080/17501911.2026.2637968","DOIUrl":"10.1080/17501911.2026.2637968","url":null,"abstract":"Sarcopenia is an age-associated degenerative disorder of skeletal muscle, characterized by the progressive decline in muscle mass and function, which increases the risk of falls, injuries, and accidental death in older adults. Deciphering its pathogenic mechanisms is crucial for advancing early detection, precision prevention, and ultimately improving the quality of life for the elderly population. Increasing evidence suggests that epigenetic regulation plays a central role in driving sarcopenia. DNA methylation, chromatin remodeling, and noncoding RNA regulation collectively accelerate the deterioration of bone and muscle by altering gene expression involved in biosynthesis and metabolism, disrupting protein homeostasis, activating inflammatory pathways, and compromising mitochondrial integrity. This review, which synthesizes the most recent progress in epigenetic research on sarcopenia, uses structured searches of PubMed and Web of Science for studies published from 2014 to the present and emphasizes how these interconnected regulatory networks drive the initiation and progression of the disease. Importantly, we emphasize their translational potential to identify novel biomarkers, enabling early risk stratification and informing the development of targeted therapeutic strategies, thereby laying the groundwork for precision clinical intervention.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"353-369"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147364507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Unlocking diagnostic potential: DNA methylation profiling in cerebrospinal fluid for central nervous system tumors. 解锁诊断潜力：中枢神经系统肿瘤脑脊液DNA甲基化谱分析

IF 2.6 4区医学

Epigenomics Pub Date : 2026-03-01 Epub Date: 2026-03-16 DOI: 10.1080/17501911.2026.2641518

Celeste Antonacci, Luana Abballe, Sara Patrizi, Evelina Miele

引用次数: 0

Epigenetic regulation in MASLD - insight for therapeutic target discovery. MASLD的表观遗传调控——对治疗靶点发现的洞察。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-03-01 Epub Date: 2026-02-25 DOI: 10.1080/17501911.2026.2633978

Jan H Britsemmer, Nuria Lopez Alcantara, Henriette Kirchner

{"title":"Epigenetic regulation in MASLD - insight for therapeutic target discovery.","authors":"Jan H Britsemmer, Nuria Lopez Alcantara, Henriette Kirchner","doi":"10.1080/17501911.2026.2633978","DOIUrl":"10.1080/17501911.2026.2633978","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease. It encompasses metabolic affections that arise primarily from lifestyle and diet, independent of alcohol consumption. Particularly, the global rise in obesity constitutes a major risk factor and comorbidity, contributing to the prevalence and severity of MASLD. Despite its widespread impact and potential progression to severe liver pathologies, effective therapies remain limited, underscoring the urgency to better understand its underlying molecular mechanisms.Epigenetic regulation is essential for maintaining hepatic metabolic function and cellular identity in response to metabolic cues but becomes critically dysregulated during MASLD. Alterations in DNA methylation, histone modifications, and non-coding RNAs contribute to disease progression, promoting metabolic dysfunction and lipid accumulation. Recent evidence indicates that epigenetic dysregulation in MASLD also occurs in a spatial manner where changes in chromatin accessibility, zone-enriched microRNAs, and transcription factor activity can disrupt gene expression along the periportal-pericentral axis, leading to zone-specific disturbances in metabolic specialization, which emerges as a critical novel factor influencing the onset and progression of MASLD. Furthermore, this review explores the role of microRNAs and extracellular vesicles in mediating systemic metabolic dysfunction observed in MASLD and highlights emerging epigenetic strategies with therapeutic potential in MASLD.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"311-333"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0