Inhibition of miR‐21 alleviated cardiac perivascular fibrosis via repressing EndMT in T1DM

• DOI: 10.1111/jcmm.14800
• Publication Date: 2019-11-04T01:49:31Z
• Authors: Qianqian Li; Yufeng Yao; Shumei Shi; Mengchen Zhou; Yingchao Zhou; Mengru Wang; Jeng‐Jiann Chiu; Zhengrong Huang; Weili Zhang; Min Liu; Qing Wang; Xin Tu
• Keywords: Diabetic Cardiomyopathy; Cardiac Fibrosis

Abstract In type 1 and 2 diabetes mellitus, increased cardiac fibrosis, stiffness associated diastolic dysfunction may be the earliest pathological phenomena in diabetic cardiomyopathy. Endothelial‐mesenchymal transition (EndMT) endothelia cells (ECs) is a critical cellular phenomenon that increases fibroblasts (CFs) fibrosis hearts. The purpose of this paper to explore molecular mechanism miR‐21 regulating EndMT perivascular vivo, hyperglycaemia up‐regulated mRNA level , aggravated collagen deposition. condition was recovered by inhibition following with improving function decreasing decreased suppressing up‐regulating SMAD7 whereas activating p‐SMAD2 p‐SMAD3. vitro, high glucose (HG) induced ECs, which . A highly conserved binding site NF‐κB located 5′‐UTR identified. directly regulated conclusion, pathway NF‐κB/ /SMAD7 process T1DM, cardiomyopathy, regarded as potential clinical therapeutic target for fibrosis.