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Methylation aberrations and genomic instability synergistically drive the evolution of intrahepatic cholangiocarcinoma. 甲基化畸变和基因组不稳定性协同驱动肝内胆管癌的进化。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-17 DOI: 10.1080/17501911.2025.2518919
Guanghao Li, Youhuang Bai, Feng Tao, Tingting Hu, Ting Wang, Yong Zeng, Deqiang Sun
{"title":"Methylation aberrations and genomic instability synergistically drive the evolution of intrahepatic cholangiocarcinoma.","authors":"Guanghao Li, Youhuang Bai, Feng Tao, Tingting Hu, Ting Wang, Yong Zeng, Deqiang Sun","doi":"10.1080/17501911.2025.2518919","DOIUrl":"https://doi.org/10.1080/17501911.2025.2518919","url":null,"abstract":"<p><strong>Aims & methods: </strong>DNA methylation and genomic instability are critical drivers of cancer initiation and malignant progression. However, the roles of methylation aberrations and genomic instability in malignant progression have not been thoroughly investigated in intrahepatic cholangiocarcinoma (ICC). To address this, we identified differentially methylated regions (DMRs) and somatic copy number alterations (SCNAs) from 341 ICC samples across various stages.</p><p><strong>Results: </strong>Our findings revealed that stages IAIB, II, IIIA, and IIIB exhibited comparable methylation changes, whereas stage IV ICC showed a pronounced accumulation of stage-specific methylation alterations. Leveraging these findings, we developed a classification model that effectively distinguished stage IV ICC from earlier stages with high accuracy using 15 DMRs. Furthermore, stage IV ICC exhibited slightly higher genomic instability, including an elevated aneuploidy score and a greater proportion of focal amplifications. We also observed a positive correlation between SCNA burden and DNA methylation entropy in the promoter, gene body, and CpG island regions, with the gene body of <i>MDM2</i> serving as a notable example.</p><p><strong>Conclusions: </strong>These findings highlight the potential of DNA methylation as a biomarker for metastasis diagnosis and the interplay between local genomic instability and aberrant methylation, emphasizing their synergistic roles in driving the evolutionary trajectory of ICC.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-14"},"PeriodicalIF":3.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316250","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
Personalized medicine for cardiovascular diseases: how next generation epigenetic technologies can contribute? 心血管疾病的个体化治疗：下一代表观遗传技术如何发挥作用？
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-14 DOI: 10.1080/17501911.2025.2518917
Meeshanthini Dogan, Robert Philibert
{"title":"Personalized medicine for cardiovascular diseases: how next generation epigenetic technologies can contribute?","authors":"Meeshanthini Dogan, Robert Philibert","doi":"10.1080/17501911.2025.2518917","DOIUrl":"https://doi.org/10.1080/17501911.2025.2518917","url":null,"abstract":"<p><p>Advances in DNA methylation and artificial intelligence have led to new methods for assessing risk and diagnosing coronary heart disease (CHD), the leading cause of death. However, whether these technologies can also be harnessed to generate new pharmacotherapeutic agents or monitor the effectiveness of new or existing CHD therapies is unknown. In this perspective, we review the development of cardiac assessment technologies and the challenges that these older approaches attempted to address. We next describe Precision Epigenetic methods and describe their strengths and limitations, as well as the conceptual framework through which these tools operate. Finally, we discuss their potential application to the development and evaluation of new therapies for CHD and how Precision Epigenetic tools compare to existing testing modalities for CHD. We conclude that the future is bright for the use of Precision Epigenetic methods in cardiovascular medicine and suggest that their routine use could lead to faster, less expensive and more effective healthcare.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-6"},"PeriodicalIF":3.0,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293477","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
The epigenetic potential of vitamin K2 in brain health. 维生素K2对大脑健康的表观遗传潜力。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-12 DOI: 10.1080/17501911.2025.2518916
Stefanos Roumeliotis, Rosaria A Cavallaro, Ioannis Kontogiorgos, Ioannis E Neofytou, Katarzyna Maresz, Jean-Francois Jeanne, Niccolò Miraglia, Andrea Fuso
{"title":"The epigenetic potential of vitamin K2 in brain health.","authors":"Stefanos Roumeliotis, Rosaria A Cavallaro, Ioannis Kontogiorgos, Ioannis E Neofytou, Katarzyna Maresz, Jean-Francois Jeanne, Niccolò Miraglia, Andrea Fuso","doi":"10.1080/17501911.2025.2518916","DOIUrl":"https://doi.org/10.1080/17501911.2025.2518916","url":null,"abstract":"<p><p>Vitamin K2 refers to a subfamily of vitamin K isoforms known as Menaquinones and, therefore, indicated as MK-n, the \"n\" indicating the number of isoprene units present in the side chain. Like the other members of the Vitamin K family, K2 is an enzymatic cofactor for the γ-glutamyl carboxylase (GGCX). This enzyme's substrates, which carboxylate glutamic acid residues, are known as Vitamin K-dependent proteins (VKDPs). Besides being involved in bone homeostasis, vitamin K exerts its primary function in the coagulation process. More recently, a function of Vitamin K also in brain homeostasis has been claimed. In addition to these so-called \"canonical\" effects, recent research highlights the possibility that Vitamin K, particularly Vitamin K2 May 2001have or induce epigenetic effects through the modulation of DNA methylation, histone modifications, and microRNAs expression. This evidence seems particularly relevant in brain diseases, where epigenetics is gaining a central role as a modulator of multiple diseases-associated molecular metabolisms. The present review examines the recent literature (PubMed) to collect evidence for the role of Vitamin K2 in neurodegenerative diseases with the goal of fostering interest in its epigenetic potential.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-10"},"PeriodicalIF":3.0,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283063","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
DNMT1/MTTP axis promotes gastritis progression during Helicobacter pylori infection by regulating GPX4 and ferroptosis. DNMT1/MTTP轴通过调节GPX4和铁下垂促进幽门螺杆菌感染期间胃炎的进展。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-09 DOI: 10.1080/17501911.2025.2510187
Chunli Tang, Fanlai Meng, Renjie Li, Meimei Ma, Meiling Zhu, Chunfang Xu
{"title":"DNMT1/MTTP axis promotes gastritis progression during <i>Helicobacter pylori</i> infection by regulating GPX4 and ferroptosis.","authors":"Chunli Tang, Fanlai Meng, Renjie Li, Meimei Ma, Meiling Zhu, Chunfang Xu","doi":"10.1080/17501911.2025.2510187","DOIUrl":"https://doi.org/10.1080/17501911.2025.2510187","url":null,"abstract":"<p><strong>Background: </strong><i>Helicobacter pylori (H. pylori)</i>-induced chronic atrophic gastritis (CAG) is a significant health concern. The role of microsomal triglyceride transfer protein (MTTP) in CAG progression has not been explored, presenting a critical knowledge gap in understanding <i>H. pylori</i>-induced CAG pathogenesis.</p><p><strong>Methods: </strong>Sprague-Dawley rats and gastric epithelial cell line were infected with H. pylori to build CAG model. The mRNA and protein levels of DNA methyltransferase 1 (DNMT1), MTTP, and glutathione peroxidase 4 (GPX4) were measured by quantitative real-time PCR (RT-qPCR) and western blotting, respectively. Moreover, the localization of DNMT1 and MTTP was detected via immunohistochemistry. Furthermore, the pathological changes of gastric tissue were analyzed by HE staining.</p><p><strong>Results: </strong>The MTTP expression was downregulated in CAG. Moreover, overexpression of MTTP in gastric epithelial cells could suppress the inflammatory response induced by <i>H. pylori</i> infection and ferroptosis by upregulating GPX4 expression. In addition, DNMT1 expression was upregulated in CAG and was negatively correlated with MTTP expression. Furthermore, DNMT1 could target MTTP promoter to activate methylation and downregulate MTTP expression.</p><p><strong>Conclusion: </strong>DNMT1 downregulated the MTTP expression through methylation, and thus mediate inflammasome-ferroptosis processes via GPX4 in the <i>H. pylori</i>-induced CAG.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-13"},"PeriodicalIF":3.0,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247087","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
Epigenetic age acceleration and psychosocial stressors in early childhood. 儿童早期的表观遗传年龄加速和社会心理压力。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-02 DOI: 10.1080/17501911.2025.2508684
Connie J Mulligan
{"title":"Epigenetic age acceleration and psychosocial stressors in early childhood.","authors":"Connie J Mulligan","doi":"10.1080/17501911.2025.2508684","DOIUrl":"https://doi.org/10.1080/17501911.2025.2508684","url":null,"abstract":"<p><p>The impact of psychosocial stress on mental and physical health is well-documented. Adverse experiences that occur early in life are particularly impactful on later life health. Epigenetic modifications, such as DNA methylation, have been proposed as a possible mechanism to mediate the impact of childhood events on adult health outcomes. The development of epigenetic clocks to estimate epigenetic age has revealed many examples of epigenetic age acceleration (and deceleration) in association with exposure to psychosocial stressors. Furthermore, altered epigenetic aging has been associated with downstream health outcomes. Here studies are discussed that have reported associations of epigenetic aging with early-life exposure to psychosocial stressors, such as childhood abuse and neglect, and with later-life health outcomes, including increased mortality, morbidity, and disease risk. Protective factors that may mitigate the effect of psychosocial stress on epigenetic aging, and possibly enable reversal of epigenetic aging, are also discussed.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-10"},"PeriodicalIF":3.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198608","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
Perspective: clinical relevance of epigenetic aging and HIV. 观点：表观遗传衰老与HIV的临床相关性。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-01 Epub Date: 2025-04-15 DOI: 10.1080/17501911.2025.2491299
Isabella C Schoepf, David Haerry, Andrés Esteban-Cantos, José R Arribas, Philip E Tarr
{"title":"Perspective: clinical relevance of epigenetic aging and HIV.","authors":"Isabella C Schoepf, David Haerry, Andrés Esteban-Cantos, José R Arribas, Philip E Tarr","doi":"10.1080/17501911.2025.2491299","DOIUrl":"10.1080/17501911.2025.2491299","url":null,"abstract":"<p><p>Longitudinal studies now document how leukocyte telomere attrition and epigenetic aging may be accelerated in people with HIV (PWH), in particular, around the time of HIV acquisition, during primary HIV infection, and during untreated chronic HIV infection. Whether chronic low-level inflammation and epigenetic aging go hand in hand or may be partially independent continues to be investigated in PWH and other settings. Epigenetic age acceleration (EAA) in PWH has now clearly been shown to be potentially reversible during successful antiretroviral therapy (ART). These studies point to how the beneficial effects of modern ART also include EAA-decelerating effects that seem large enough to regard ART as a kind of epigenetic rejuvenation therapy. Progress in the field has been limited in part due to the high cost of assessing EAA based on DNA methylation measures (\"epigenetic clocks\"). Demonstration of the clinical relevance of EAA and its reversion by ART will depend on large studies associating EAA with cardiovascular events and other adverse aging-associated endpoints in PWH.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"523-527"},"PeriodicalIF":3.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959836","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
Statement of Retraction: KDM6B Histone Demethylase is an Epigenetic Regulator of Estrogen Receptor β Expression in Human Pleural Mesothelioma. 撤回声明：KDM6B组蛋白去甲基化酶是人胸膜间皮瘤中雌激素受体β表达的表观遗传调节剂。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-01 Epub Date: 2025-06-05 DOI: 10.1080/17501911.2025.2514326
{"title":"Statement of Retraction: KDM6B Histone Demethylase is an Epigenetic Regulator of Estrogen Receptor β Expression in Human Pleural Mesothelioma.","authors":"","doi":"10.1080/17501911.2025.2514326","DOIUrl":"10.1080/17501911.2025.2514326","url":null,"abstract":"","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":"17 9","pages":"645"},"PeriodicalIF":3.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224800","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
Epigenetic insights of olanzapine-induced insulin resistance. 奥氮平诱发胰岛素抵抗的表观遗传学启示。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-01 Epub Date: 2025-04-04 DOI: 10.1080/17501911.2025.2489341
David Frond, Adam Rettig, Kyle Burghardt
{"title":"Epigenetic insights of olanzapine-induced insulin resistance.","authors":"David Frond, Adam Rettig, Kyle Burghardt","doi":"10.1080/17501911.2025.2489341","DOIUrl":"10.1080/17501911.2025.2489341","url":null,"abstract":"","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"507-509"},"PeriodicalIF":3.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788176","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
Mom genes and dad genes: genomic imprinting in the regulation of social behaviors. 母亲基因和父亲基因：社会行为调控中的基因组印记。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-01 Epub Date: 2025-04-18 DOI: 10.1080/17501911.2025.2491294
Erin M O'Leary, Paul J Bonthuis
{"title":"Mom genes and dad genes: genomic imprinting in the regulation of social behaviors.","authors":"Erin M O'Leary, Paul J Bonthuis","doi":"10.1080/17501911.2025.2491294","DOIUrl":"10.1080/17501911.2025.2491294","url":null,"abstract":"<p><p>Genomic imprinting is an epigenetic phenomenon in mammals that affects brain development and behavior. Imprinting involves the regulation of allelic expression for some genes in offspring that depends on whether alleles are inherited from mothers compared to fathers, and is thought to provide parental control over offspring social behavior phenotypes. Imprinted gene expression is prevalent in the mammalian brain, and human imprinted gene mutations are associated with neurodevelopmental disorders and neurodivergent social behavior in Prader-Willi Syndrome, Angelman Syndrome, and autism. Here, we provide a review of the evidence that imprinted genes influence social behaviors across major neurodevelopmental stages in humans and mouse animal models that include parent-infant interactions, juvenile sociability, and adult aggression, dominance, and sexual behavior.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"555-573"},"PeriodicalIF":3.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985838","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
Selective chemical tracking of DNA methylomes in live cells. 活细胞中DNA甲基化组的选择性化学跟踪。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-01 Epub Date: 2025-05-06 DOI: 10.1080/17501911.2025.2500914
Vaidotas Stankevičius, Liepa Gasiulė, Giedrius Vilkaitis, Saulius Klimašauskas
{"title":"Selective chemical tracking of DNA methylomes in live cells.","authors":"Vaidotas Stankevičius, Liepa Gasiulė, Giedrius Vilkaitis, Saulius Klimašauskas","doi":"10.1080/17501911.2025.2500914","DOIUrl":"10.1080/17501911.2025.2500914","url":null,"abstract":"","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"575-577"},"PeriodicalIF":3.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004340","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
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