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

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

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

2025
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Overview
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. •Transcriptome analysis of myocardial tissues revealed a dramatic up-regulation of the TGF-β1/Smad pathway•In vitro studies showed that EDA attenuated myocardial fibrosis by inhibiting the TGF-β1/Smad signaling pathway and its downstream fibrosis key factors, Col3a1 and α-SMA.