{"title":"口服依达拉奉通过TGF-β1/Smad信号通路改善2型糖尿病大鼠心肌纤维化","authors":"Xiao-Yan Zhang , Yong-xuan Xu , Si-Quan Xue , Yue-Qin Zeng , Juan-Hua Gu , Xin-Fu Zhou , Hai-Yun Luo , Li-Jin Pu","doi":"10.1016/j.jdiacomp.2025.108976","DOIUrl":null,"url":null,"abstract":"<div><div>Myocardial fibrosis, characterized by increased reactive oxygen species (ROS), is a key pathological feature of diabetic cardiomyopathy (DCM). Although oral edaravone (EDA) shows therapeutic potential in ameliorating myocardial fibrosis in DCM, the precise mechanisms remain unclear. Transcriptome analysis of myocardial tissues revealed a dramatic up-regulation of the TGF-β1/Smad pathway, which was reversed by oral EDA treatment. In vitro studies showed that oral EDA attenuated myocardial fibrosis by inhibiting the TGF-β1/Smad signaling pathway and its downstream fibrosis key factors, Col3a1 and α-SMA. These findings suggest that oral EDA improves myocardial fibrosis in Type 2 diabetes mellitus (T2DM) by inhibiting the TGF-β1/Smad signaling pathway and holds promise as an effective treatment for myocardial fibrosis in DCM.</div></div>","PeriodicalId":15659,"journal":{"name":"Journal of diabetes and its complications","volume":"39 3","pages":"Article 108976"},"PeriodicalIF":2.9000,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Oral edaravone ameliorates myocardial fibrosis in type 2 diabetic rats by TGF-β1/Smad signaling pathway\",\"authors\":\"Xiao-Yan Zhang , Yong-xuan Xu , Si-Quan Xue , Yue-Qin Zeng , Juan-Hua Gu , Xin-Fu Zhou , Hai-Yun Luo , Li-Jin Pu\",\"doi\":\"10.1016/j.jdiacomp.2025.108976\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Myocardial fibrosis, characterized by increased reactive oxygen species (ROS), is a key pathological feature of diabetic cardiomyopathy (DCM). Although oral edaravone (EDA) shows therapeutic potential in ameliorating myocardial fibrosis in DCM, the precise mechanisms remain unclear. Transcriptome analysis of myocardial tissues revealed a dramatic up-regulation of the TGF-β1/Smad pathway, which was reversed by oral EDA treatment. In vitro studies showed that oral EDA attenuated myocardial fibrosis by inhibiting the TGF-β1/Smad signaling pathway and its downstream fibrosis key factors, Col3a1 and α-SMA. These findings suggest that oral EDA improves myocardial fibrosis in Type 2 diabetes mellitus (T2DM) by inhibiting the TGF-β1/Smad signaling pathway and holds promise as an effective treatment for myocardial fibrosis in DCM.</div></div>\",\"PeriodicalId\":15659,\"journal\":{\"name\":\"Journal of diabetes and its complications\",\"volume\":\"39 3\",\"pages\":\"Article 108976\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2025-02-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of diabetes and its complications\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1056872725000297\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of diabetes and its complications","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1056872725000297","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
Oral edaravone ameliorates myocardial fibrosis in type 2 diabetic rats by TGF-β1/Smad signaling pathway
Myocardial fibrosis, characterized by increased reactive oxygen species (ROS), is a key pathological feature of diabetic cardiomyopathy (DCM). Although oral edaravone (EDA) shows therapeutic potential in ameliorating myocardial fibrosis in DCM, the precise mechanisms remain unclear. Transcriptome analysis of myocardial tissues revealed a dramatic up-regulation of the TGF-β1/Smad pathway, which was reversed by oral EDA treatment. In vitro studies showed that oral EDA attenuated myocardial fibrosis by inhibiting the TGF-β1/Smad signaling pathway and its downstream fibrosis key factors, Col3a1 and α-SMA. These findings suggest that oral EDA improves myocardial fibrosis in Type 2 diabetes mellitus (T2DM) by inhibiting the TGF-β1/Smad signaling pathway and holds promise as an effective treatment for myocardial fibrosis in DCM.
期刊介绍:
Journal of Diabetes and Its Complications (JDC) is a journal for health care practitioners and researchers, that publishes original research about the pathogenesis, diagnosis and management of diabetes mellitus and its complications. JDC also publishes articles on physiological and molecular aspects of glucose homeostasis.
The primary purpose of JDC is to act as a source of information usable by diabetes practitioners and researchers to increase their knowledge about mechanisms of diabetes and complications development, and promote better management of people with diabetes who are at risk for those complications.
Manuscripts submitted to JDC can report any aspect of basic, translational or clinical research as well as epidemiology. Topics can range broadly from early prediabetes to late-stage complicated diabetes. Topics relevant to basic/translational reports include pancreatic islet dysfunction and insulin resistance, altered adipose tissue function in diabetes, altered neuronal control of glucose homeostasis and mechanisms of drug action. Topics relevant to diabetic complications include diabetic retinopathy, neuropathy and nephropathy; peripheral vascular disease and coronary heart disease; gastrointestinal disorders, renal failure and impotence; and hypertension and hyperlipidemia.