{"title":"DNA methyltransferase 1-mediated methylation of midkine regulate myocardial ischemia-reperfusion injury via the Notch2/Hes1 axis.","authors":"Wei Liu, Yuqin Wang, Jiayuan Wu, Caihong He, Zhengwei Zhou","doi":"10.1080/08977194.2025.2595011","DOIUrl":null,"url":null,"abstract":"<p><p>myocardial ischemia-reperfusion injury (MI/RI) threatens people's lives. Midkine (MDK) has a protective effect against MI/RI. DNA methyltransferase 1 (DNMT1) is closely associated with MI/RI. Mouse cardiomyocytes were isolated to establish a model of myocardial ischemia-reperfusion. Subsequently, the viability, apoptosis, and inflammatory factors of the cardiomyocytes treated under different conditions were measured. Western blotting was employed to examine the expression of related proteins. Chromatin immunoprecipitation (CHIP) and dual-luciferase reporter gene assays were conducted to verify the relationships among the DNMT1, MDK, and Notch2/Hes1 signaling pathways. The expression of MDK was reduced in the MI/RI cell model, while Notch2/Hes1 was activated. Overexpression of MDK mitigated the injury associated with MI/RI. Methylation modification of DNMT1 downregulated MDK, thereby mediating the Notch2/Hes1 pathway. The methylation modification of DNMT1 on MDK regulated the progression of MI/RI. The methylation modification of MDK by DNMT1 likely downregulates the Notch2/Hes1 pathway, thereby influencing MI/RI.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"203-215"},"PeriodicalIF":1.9000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Growth factors","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/08977194.2025.2595011","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/12/4 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
myocardial ischemia-reperfusion injury (MI/RI) threatens people's lives. Midkine (MDK) has a protective effect against MI/RI. DNA methyltransferase 1 (DNMT1) is closely associated with MI/RI. Mouse cardiomyocytes were isolated to establish a model of myocardial ischemia-reperfusion. Subsequently, the viability, apoptosis, and inflammatory factors of the cardiomyocytes treated under different conditions were measured. Western blotting was employed to examine the expression of related proteins. Chromatin immunoprecipitation (CHIP) and dual-luciferase reporter gene assays were conducted to verify the relationships among the DNMT1, MDK, and Notch2/Hes1 signaling pathways. The expression of MDK was reduced in the MI/RI cell model, while Notch2/Hes1 was activated. Overexpression of MDK mitigated the injury associated with MI/RI. Methylation modification of DNMT1 downregulated MDK, thereby mediating the Notch2/Hes1 pathway. The methylation modification of DNMT1 on MDK regulated the progression of MI/RI. The methylation modification of MDK by DNMT1 likely downregulates the Notch2/Hes1 pathway, thereby influencing MI/RI.
期刊介绍：
Growth Factors is an international and interdisciplinary vehicle publishing new knowledge and findings on the regulators of cell proliferation, differentiation and survival. The Journal will publish research papers, short communications and reviews on current developments in cell biology, biochemistry, physiology or pharmacology of growth factors, cytokines or hormones which improve our understanding of biology or medicine. Among the various fields of study topics of particular interest include: •Stem cell biology •Growth factor physiology •Structure-activity relationships •Drug development studies •Clinical applications
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