Oral edaravone ameliorates myocardial fibrosis in type 2 diabetic rats by TGF-β1/Smad signaling pathway
Date
2025
Authors
Zhang, X.Y.
Xu, Y.X.
Xue, S.Q.
Zeng, Y.Q.
Gu, J.H.
Zhou, X.F.
Luo, H.Y.
Pu, L.J.
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Journal article
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Journal of Diabetes and its Complications, 2025; 39(3):1-11
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Abstract
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.
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Copyright 2025 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies.