The metastasis-associated protein MTA3 promotes cardiac repair by inhibiting the fibroblast to myofibroblast transition during fibrosis.

ABSTRACT: Cardiac fibrosis is a pathological hallmark of various cardiovascular disorders. Accumulating evidence has demonstrated that fibroblasts transform into myofibroblasts during the occurrence of cardiac fibrosis, but the mechanism remains incompletely understood. This study aims to investigate the relevance of MTA3 as a potential therapeutic target for cardiac fibrosis. The myocardial infarction model was established by ligating the left coronary artery of C57BL6 mice, and myocardial fibrosis was measured by cardiac ultrasound and Sirius red staining of myocardium. MTA3 overexpression plasmid was constructed and transfected into primary fibroblasts, immunofluorescence, Western blot and qRT-PCR were used to detect the expression of MTA3, α-SMA, and Collagen I. RNAi was used to interfere with t

SUBMITTER: Wang X 

PROVIDER: S-EPMC12319557 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature