Oral edaravone ameliorates myocardial fibrosis in type 2 diabetic rats by TGF-β1/Smad signaling pathway

被引:0
|
作者
Zhang, Xiao-Yan [1 ]
Xu, Yong-xuan [1 ]
Xue, Si-Quan [2 ]
Zeng, Yue-Qin [2 ]
Gu, Juan-Hua [2 ]
Zhou, Xin-Fu [3 ,4 ]
Luo, Hai-Yun [1 ,5 ]
Pu, Li-Jin [1 ,6 ]
机构
[1] Kunming Med Univ, Affiliated Hosp 1, Fac Basic Med Sci, Dept Cardiol, 296 Xichang Rd, Kunming 650032, Peoples R China
[2] Biomed Engn Res Ctr, Yunnan Key Lab Stem Cells & Regenerat Med, 1168 Chunrong West Rd, Kunming 650500, Peoples R China
[3] Suzhou Auzone Biotech, Suzhou, Peoples R China
[4] Univ South Australia, Hlth & Biomed Innovat, Clin & Hlth Sci, 101 Currie St, Adelaide 5001, Australia
[5] Kunming Med Univ, Fac Basic Med Sci, 1168 Chunrong West Rd, Kunming 650500, Peoples R China
[6] Kunming Med Univ, Affiliated Hosp 1, 296 Xichang Rd, Kunming 650032, Peoples R China
关键词
TGF-beta 1/Smad signaling pathway; Edaravone; Myocardial fibrosis; Type 2 diabetes mellitus; GROWTH-FACTOR-BETA; OXIDATIVE STRESS; CARDIAC FIBROSIS; CARDIOMYOPATHY; ANTIOXIDANT; AUTOPHAGY; DAMAGE; SCAR;
D O I
10.1016/j.jdiacomp.2025.108976
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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-(31/Smad pathway, which was reversed by oral EDA treatment. In vitro studies showed that oral EDA attenuated myocardial fibrosis by inhibiting the TGF-(31/Smad signaling pathway and its downstream fibrosis key factors, Col3a1 and a-SMA. These findings suggest that oral EDA improves myocardial fibrosis in Type 2 diabetes mellitus (T2DM) by inhibiting the TGF-(31/Smad signaling pathway and holds promise as an effective treatment for myocardial fibrosis in DCM.
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页数:11
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