MicroRNA-130a attenuates cardiac fibrosis after myocardial infarction through TGF-β/Smad signaling by directly targeting TGF-β receptor 1
Feng Yu, Yintu Bao, Jiaxing Ding, Huili Li, Wei Liu, Xuehua Wang, Hongquan Guan, Zhijian Chen
Abstract
was a target gene of miR-130a. miR-130a inhibition heightened Col-1, α-SMA, and TGFBR1 expressions and Smad3 phosphorylation levels in CFs; however, these increments were suppressed by the overexpression of miR-130a. Meanwhile, co-transfection with TGFBR1 weakened miR-130a's ability to inhibit α-SMA and Col-1 expression. These findings suggest that miR-130a exerts antifibrotic properties by directly targeting TGFBR1 to regulate TGF-β/Smad signaling and inhibit the conversion of CFs to myofibroblasts. Thus, miR-130a is a promising therapeutic target for alleviating cardiac fibrosis.
Topics & Concepts
SMADCardiac fibrosisFibrosisMyocardial fibrosismicroRNATransforming growth factorMyofibroblastSignal transductionMedicineDownregulation and upregulationCancer researchInternal medicineCell biologyChemistryBiologyGeneBiochemistryCardiac Fibrosis and RemodelingSignaling Pathways in DiseaseCardiac Valve Diseases and Treatments