Epigenomics最新文献_第4页

HOTAIR at the metabolic crossroads: lncRNA control of carbohydrate and lipid metabolism. HOTAIR在代谢的十字路口：lncRNA控制碳水化合物和脂质代谢。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-07-01 Epub Date: 2026-07-03 DOI: 10.1080/17501911.2026.2691028

Julio Sánchez-Pérez, Samuel Trujano-Camacho, Verónica García-Castillo, Mercedes Olvera-Valencia, David Cantú de León, Eduardo López-Urrutia, Carlos Pérez-Plasencia

{"title":"HOTAIR at the metabolic crossroads: lncRNA control of carbohydrate and lipid metabolism.","authors":"Julio Sánchez-Pérez, Samuel Trujano-Camacho, Verónica García-Castillo, Mercedes Olvera-Valencia, David Cantú de León, Eduardo López-Urrutia, Carlos Pérez-Plasencia","doi":"10.1080/17501911.2026.2691028","DOIUrl":"10.1080/17501911.2026.2691028","url":null,"abstract":"Cancer cells reprogram their metabolic networks to sustain continuous proliferation, resist stress, and support invasive behavior. This metabolic rewiring includes enhanced aerobic glycolysis, increased glutaminolysis to fuel biosynthetic reactions, activation of the pentose phosphate pathway (PPP) for nucleotide synthesis and redox balance, and reorganization of lipid metabolism to integrate membrane biogenesis and energy adaptation. While several oncogenes are well established as metabolic regulators, it is increasingly recognized that non-coding RNAs also contribute to the control of tumor metabolic phenotypes. Among them, the long non-coding RNA (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) has emerged as one of the most consistently upregulated and functionally relevant lncRNAs in human cancers. Accumulating evidence links HOTAIR to metabolic reprogramming in diverse tumor types. HOTAIR controls the expression and activity of key glycolytic enzymes and regulates lipogenesis, lipid accumulation, and metastatic lipid remodeling. However, findings remain dispersed across individual studies, and a consolidated framework integrating HOTAIR regulation with major metabolic pathways is currently lacking. This review synthesizes current knowledge on how HOTAIR drives metabolic rewiring in cancer, with a focus on carbohydrate and lipid metabolism, and discusses the underlying molecular mechanisms and therapeutic implications.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"911-921"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374779","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

DNA methylation quality control decisions, removed beta values, and their influence on epigenetic clocks. DNA甲基化质量控制决策，去除β值，及其对表观遗传时钟的影响。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-07-01 Epub Date: 2026-07-20 DOI: 10.1080/17501911.2026.2698008

Audrey L Kelly, Brandt Levitt, Allison Aiello, Chantel L Martin, Kathleen Mullan Harris, Lauren Gaydosh

{"title":"DNA methylation quality control decisions, removed beta values, and their influence on epigenetic clocks.","authors":"Audrey L Kelly, Brandt Levitt, Allison Aiello, Chantel L Martin, Kathleen Mullan Harris, Lauren Gaydosh","doi":"10.1080/17501911.2026.2698008","DOIUrl":"10.1080/17501911.2026.2698008","url":null,"abstract":"Background: Measures of biological aging based on DNA methylation (epigenetic clocks) are commonly used in research across the biological, health, and social sciences. Many decisions are made during the quality control (QC) of the data on which such clocks are based, generating removed beta values that must be accommodated in construction of the clocks.Methods: We apply a range of detection p-value and bead count thresholds during QC of a DNA methylation dataset and characterize the removed beta values. We then test different methods of imputing removed beta values and their impact on epigenetic clocks.Results: We find that both detection p-value and bead count thresholds remove beta values that differ significantly in their distribution from the values retained post-QC. Epigenetic clocks calculated from datasets using various imputation methods (mean, median, KNN, and methyLImp) do not appear to have consistent patterns of bias. The only exception is imputation of 0 for removed beta values (akin to leaving out those CpGs on a per-sample basis when calculating clocks), which shows stronger proportional bias of clock values for all clocks.Conclusion: We recommend imputing removed beta values rather than leaving those CpGs out of clock calculations on a per-sample basis.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"821-831"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148519997","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

Clinical diagnostic utility of MGMT promoter methylation. MGMT启动子甲基化的临床诊断价值。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-07-01 Epub Date: 2026-06-17 DOI: 10.1080/17501911.2026.2688974

Ulrich Lehmann

{"title":"Clinical diagnostic utility of MGMT promoter methylation.","authors":"Ulrich Lehmann","doi":"10.1080/17501911.2026.2688974","DOIUrl":"10.1080/17501911.2026.2688974","url":null,"abstract":"Tumor suppressor genes and DNA repair genes can be inactivated not only by genetic lesions, like mutations or deletions, but also by aberrant DNA methylation of promoter regions. These DNA methylation alterations may serve as biomarkers for early detection, refinement of diagnosis, prognosis, or prediction of therapy response. Despite a long history of DNA methylation research in the field of oncology so far only very few aberrant DNA methylation events are of proven and generally accepted clinical value and are part of the routine diagnostic work‑up of cancer patient samples. Hypermethylation of the MGMT gene promoter in glioblastoma is one of the very few DNA methylation biomarkers that has entered routine clinical diagnostics. In this very aggressive primary brain tumor it is associated with an overall better prognosis and a better response to alkylating therapy. This narrative review provides an overview about the underlying biology, the methodological challenges, and the clinical utility of MGMT promoter methylation, primarily in the context of glioblastoma. Emerging applications in other cancer types are also summarized and discussed. Throughout the review the focus is more on a critical discussion of concepts and relevant publications and their merits and shortcomings than trying to achieve complete coverage of the voluminous literature.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"877-888"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263824","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

Global 5-methylcytosine and 5-hydroxymethylcytosine levels and their clinical associations in metabolic syndrome. 代谢综合征患者5-甲基胞嘧啶和5-羟甲基胞嘧啶水平及其临床相关性

IF 3.1 4区医学

Epigenomics Pub Date : 2026-07-01 Epub Date: 2026-07-09 DOI: 10.1080/17501911.2026.2700472

Sacide Pehlivan, Yasemin Oyaci, Naci Şenkal, Ebru Teberik Kama, Mustafa Pehlivan, Tufan Tükek, Alpay Medetalibeyoğlu

{"title":"Global 5-methylcytosine and 5-hydroxymethylcytosine levels and their clinical associations in metabolic syndrome.","authors":"Sacide Pehlivan, Yasemin Oyaci, Naci Şenkal, Ebru Teberik Kama, Mustafa Pehlivan, Tufan Tükek, Alpay Medetalibeyoğlu","doi":"10.1080/17501911.2026.2700472","DOIUrl":"10.1080/17501911.2026.2700472","url":null,"abstract":"Purpose: Metabolic syndrome (MetS) is a complex condition characterized by multiple metabolic abnormalities, in which epigenetic regulation has been increasingly implicated. This study aimed to evaluate global DNA methylation markers, 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC), in individuals with MetS and examine their associations with clinical and biochemical parameters.Methods: A total of 200 patients with MetS and 103 healthy controls were included. Global 5-mC and 5-hmC levels were compared between groups. In the MetS group, correlations between these markers and metabolic, renal, and endocrine parameters were assessed using Spearman correlation analysis.Results: Global 5-mC levels were significantly higher in MetS patients than in controls (p < 0.001), whereas global 5-hmC levels did not differ between groups. However, 5-hmC levels were negatively correlated with body weight, glycated hemoglobin (HbA1c), triglycerides, creatinine, and thyroid-stimulating hormone (TSH), and positively correlated with high-density lipoprotein cholesterol (HDL-C) and free thyroxine (free T4). In contrast, 5-mC levels showed limited associations with clinical parameters.Conclusion: Global 5-mC levels are elevated in MetS, whereas 5-hmC levels remain unchanged. The broader associations of 5-hmC with clinical and biochemical parameters suggest that hydroxymethylation may provide complementary insight into metabolic heterogeneity in MetS.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"833-841"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410810","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

RNF125 inhibits EMT and glycolysis in breast cancer by suppressing HDAC1-mediated histone deacetylation of PGM5. RNF125通过抑制hdac1介导的PGM5组蛋白去乙酰化抑制乳腺癌的EMT和糖酵解。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-07-01 Epub Date: 2026-07-14 DOI: 10.1080/17501911.2026.2696955

Yanhong Wei, Zhaohui Tang, Pengfei Luo, Yongjian Chen, Zuneng He, Zhangwen Tang, Lin Liao, Fang Li, Xuanye Ouyang, Ming Wu, Shaohui Jiang, Sijuan Ding

{"title":"RNF125 inhibits EMT and glycolysis in breast cancer by suppressing HDAC1-mediated histone deacetylation of PGM5.","authors":"Yanhong Wei, Zhaohui Tang, Pengfei Luo, Yongjian Chen, Zuneng He, Zhangwen Tang, Lin Liao, Fang Li, Xuanye Ouyang, Ming Wu, Shaohui Jiang, Sijuan Ding","doi":"10.1080/17501911.2026.2696955","DOIUrl":"10.1080/17501911.2026.2696955","url":null,"abstract":"Background: Epithelial-mesenchymal transition (EMT) and glycolysis contribute to breast cancer (BC). However, the molecular mechanisms underlying these processes require further investigation.Methods: Gene abundance was determined using RT-qPCR, Western blotting, and IHC. Cell viability and migration were evaluated using CCK-8 and scratch tests. Co-IP was performed to confirm the RNF125-HDAC1 interaction. Glycolysis-related indicators were detected using commercial kits, the Seahorse XF assay, and Western blotting. The enrichment of H3K27ac in the PGM5 promoter was determined using ChIP.Results: In BC samples, RNF125 and PGM5 levels were downregulated, whereas HDAC1 expression was upregulated. Upregulation of RNF125 inhibited EMT and glycolysis in BC cells, suppressed tumor growth in subcutaneous tumor-bearing mouse models, and reduced lung metastasis in mice; these effects were counteracted by HDAC1 overexpression. Similarly, PGM5 overexpression suppressed EMT and glycolysis in BC cells; however, this suppression was blocked by HDAC1 overexpression or RNF125 knockdown. Mechanistically, RNF125 promoted HDAC1 ubiquitination, leading to its proteasomal degradation. Moreover, HDAC1 reduced PGM5 expression by inhibiting H3K27ac enrichment at the PGM5 promoter.Conclusion: RNF125 suppressed EMT and glycolysis in BC cells and delayed tumor growth in subcutaneous tumor-bearing mouse models, as well as lung metastasis in mice through modulation of the HDAC1/PGM5 axis.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"791-803"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435639","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

Promoter methylation-associated brain-enriched long noncoding RNAs in glioblastoma: a multi-cohort public epigenomic re-analysis. 胶质母细胞瘤中启动子甲基化相关的大脑富集长链非编码rna：一项多队列公开表观基因组重新分析。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-07-01 Epub Date: 2026-06-19 DOI: 10.1080/17501911.2026.2691031

Ye Tan, Fengyu Cheng, Pu Li, Jingxuan Xiang, Yuhong Tang, Aidong Chen, Peiying Han

{"title":"Promoter methylation-associated brain-enriched long noncoding RNAs in glioblastoma: a multi-cohort public epigenomic re-analysis.","authors":"Ye Tan, Fengyu Cheng, Pu Li, Jingxuan Xiang, Yuhong Tang, Aidong Chen, Peiying Han","doi":"10.1080/17501911.2026.2691031","DOIUrl":"10.1080/17501911.2026.2691031","url":null,"abstract":"Background: Glioblastoma (GBM) is epigenetically heterogeneous, and previous long noncoding RNA (lncRNA) methylation studies have often begun from tumor-wide screens. We asked whether brain-enriched lncRNAs show promoter methylation-associated suppression in GBM.Research design and methods: Brain-enriched lncRNAs were defined using GENCODE v49 and GTEx/UCSC Xena. Primary discovery used TCGA-GBM primary tumors with matched expression and promoter methylation; 52 patients had both data types. Spearman correlations identified methylation-associated candidates (ρ ≤-0.30; false discovery rate [FDR] < 0.05). External layers used GSE36278 methylation, CGGA expression/survival, and GSE131928 Smart-seq2 state scores.Results: Of 13,213 lncRNAs, 437 were brain-enriched and 76 entered matched TCGA analysis; seven met core criteria. PTPRD-AS1 and NFIB-AS1 showed the strongest inverse coupling (ρ = -0.665 and -0.639; FDR = 0.000016 and 0.000028). GSE36278 supported hypermethylation direction for all seven candidates, with six FDR-significant. MEG8 and FAM201A were downregulated in CGGA versus GTEx brain, and FAM201A associated with pseudobulk stemness and mesenchymal scores.Conclusions: This public-data re-analysis prioritizes brain-enriched lncRNAs associated with promoter hypermethylation and lower expression in GBM, but does not establish direct methylation-mediated silencing.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"781-790"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276564","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

Transposable element regulation in mammalian germ cells and other contexts: multilayered repression, fertility, and regulated activation. 转座因子在哺乳动物生殖细胞和其他环境中的调控：多层抑制、生育和调控激活。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-07-01 Epub Date: 2026-06-10 DOI: 10.1080/17501911.2026.2685055

Peilin Li, Soichiro Yamanaka

{"title":"Transposable element regulation in mammalian germ cells and other contexts: multilayered repression, fertility, and regulated activation.","authors":"Peilin Li, Soichiro Yamanaka","doi":"10.1080/17501911.2026.2685055","DOIUrl":"10.1080/17501911.2026.2685055","url":null,"abstract":"Transposable elements (TEs), particularly retrotransposons that dominate mammalian genomes, are pervasive components of mammalian genomes whose activation is constrained by multilayered repression systems. In germ cells, this repression architecture is particularly elaborate, integrating chromatin-based silencing, DNA methylation, and small RNA-guided pathways to safeguard genome integrity during epigenetic reprogramming. These mechanisms are coordinated yet mechanistically specialized, targeting distinct phases of the transposon life cycle and different TE families across developmental stages. Yet the distinctive chromatin landscape of germ cells also creates windows of developmental permissiveness during which TE transcription can occur. Beyond the germline, TE expression can emerge in defined stages of early embryogenesis, extraembryonic development, neural differentiation, and aging, with consequences ranging from chromatin remodeling and regulatory co-option to inflammatory signaling and genome instability. Together, these observations raise a central question: how do different mammalian lineages balance epigenetic plasticity with genome defense? Here, we synthesize current understanding of the molecular logic of TE repression, emphasizing the germline, and integrate evidence across development and aging. We highlight shared principles-such as epigenetic permissiveness and RNA-guided targeting-while underscoring a key difference in regulatory outcome: somatic contexts may tolerate, co-opt, or pathologically amplify TE activity, whereas the germline converts transient activation into heritable, sequence-specific silencing.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"843-860"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148210669","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

Long-term molecular embedding of early life adversity: leukocyte DNA methylation and gene expression associations from childhood to young adulthood. 早期生活逆境的长期分子嵌入：从童年到成年早期白细胞DNA甲基化和基因表达的关联。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-07-01 Epub Date: 2026-06-27 DOI: 10.1080/17501911.2026.2694424

Saher Daredia, Dennis Khodasevich, Anne K Bozack, Rosemarie de la Rosa, Katherine R Kogut, Nina Holland, Brenda Eskenazi, Julianna Deardorff, Andres Cardenas

{"title":"Long-term molecular embedding of early life adversity: leukocyte DNA methylation and gene expression associations from childhood to young adulthood.","authors":"Saher Daredia, Dennis Khodasevich, Anne K Bozack, Rosemarie de la Rosa, Katherine R Kogut, Nina Holland, Brenda Eskenazi, Julianna Deardorff, Andres Cardenas","doi":"10.1080/17501911.2026.2694424","DOIUrl":"10.1080/17501911.2026.2694424","url":null,"abstract":"Background: Early life adversity is associated with increased cardiometabolic risk across the life course, potentially via epigenetic mechanisms. However, few studies have prospectively examined how distinct domains of early life adversity influence molecular profiles and cardiometabolic health.Research design and methods: In the CHAMACOS cohort, a longitudinal study of rural Latino youth, we measured adversity prospectively from pregnancy through age 7 across six domains: Learning Environment, Parent-Child Interaction, Maternal Adversity, Family Dysfunction, Economic Adversity, and Stressful Life Events. Leukocyte DNA methylation (DNAm) was measured at four timepoints between ages 7 and 18, gene expression (RNA transcripts) at age 14, and body mass index (BMI) and insulin resistance (HOMA-IR) at age 18.Results: Early life adversity was associated with differential DNAm at ages 7, 14, and 18, with 14 Bonferroni- and 101 FDR-significant differentially methylated probes (DMPs) across all timepoints. Economic adversity was the domain most strongly associated with DMPs (4 Bonferroni- and 38 FDR-significant). Methylation changes at several DMPs were significantly associated with BMI and HOMA-IR at age 18.Conclusions: These findings provide longitudinal evidence that early life adversity, particularly economic adversity, becomes biologically embedded via DNAm, with functional and cardiometabolic consequences, highlighting potential targets for early interventions to reduce lifelong disease risk.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"805-820"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337916","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

Dual epigenetic targeting in neuroblastoma: a new paradigm from synergistic lethality to clinical translation. 神经母细胞瘤的双重表观遗传靶向：从协同致死性到临床转化的新范式。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-06-01 Epub Date: 2026-05-14 DOI: 10.1080/17501911.2026.2671148

Diana Treis, Conny Tümmler, John Inge Johnsen

引用次数: 0

Human DNA methylation biomarkers in diabetic complications: from association to clinical translation. 糖尿病并发症中的人类DNA甲基化生物标志物：从关联到临床转化。

IF 3.1 4区医学

Epigenomics Pub Date : 2026-06-01 Epub Date: 2026-05-26 DOI: 10.1080/17501911.2026.2678921

Ishant Khurana, Ram Abou Zaki, Assam El-Osta

{"title":"Human DNA methylation biomarkers in diabetic complications: from association to clinical translation.","authors":"Ishant Khurana, Ram Abou Zaki, Assam El-Osta","doi":"10.1080/17501911.2026.2678921","DOIUrl":"10.1080/17501911.2026.2678921","url":null,"abstract":"Diabetic complications are a major contributor to morbidity and mortality, yet accurately identifying individuals at highest risk remains a persistent clinical challenge. Although established clinical risk factors underpin current prediction models, their ability to forecast complication onset and progression remains limited. Long-term follow-up of landmark clinical trials revealed the phenomenon of metabolic memory, whereby early glycemic exposure leaves a lasting imprint on future complication risk, even after glycemic differences have converged. Epigenetic mechanisms are compelling mediators of this effect, as they encode stable changes in gene regulation without altering the underlying DNA sequence.Over the past decade, human studies have linked epigenetic modifications, particularly DNA methylation, to diabetic complications, yet translation into clinically useful biomarkers has been slow. This Perspective examines the current landscape of human epigenetic biomarker research, highlighting both biological insights and methodological constraints. We discuss key technological platforms, including Infiniummethylation arrays and sequencing-based approaches such as bisulfites sequencing and enzymatic methyl-sequencing (EM-seq). While earlyarray-based studies provided proof of concept, next-generation sequencing approaches offer substantially greater discovery potential.We conclude by outlining priorities for the next decade, emphasizing longitudinal cohorts, multi-omics integration, and predictive frameworks capable oftransforming epigenetic signals into meaningful clinical tools.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"723-737"},"PeriodicalIF":3.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148028413","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