Targeting SYK with miR-512-3p provides therapeutic potential in myocardial fibrosis.

ABSTRACT: Myocardial fibrosis is a key pathological process in cardiovascular diseases. The activation of myocardial fibroblasts has been shown to be regulated by several signalling pathways, including Ang II signalling pathway. This study aimed to investigate the role of SYK (spleen tyrosine kinase) in myocardial fibrosis and explore its upstream regulator targeting SYK expression. In an isoproterenol (ISO)-induced myocardial fibrosis murine model, SYK was highly expressed in activated myocardial fibroblasts and colocalized with α-SMA. In vitro, Ang II stimulation increased the levels of SYK and its phosphorylated form, promoting fibroblast activation and ECM protein secretion. SYK knockdown effectively inhibited fibroblast activation in HL-1 cells. Bioinformatics analysis and functional screening

SUBMITTER: Li W 

PROVIDER: S-EPMC12569063 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature