Highlight
– Secreted modular calcium-binding protein 1 (SMOC-1) is significantly upregulated in patients with acute myocardial infarction (AMI) complicated by cardiac rupture.
– Cardiomyocyte-derived SMOC-1 promotes reparative fibrosis by activating cardiac fibroblasts, enhancing collagen synthesis and maturation.
– Cardiomyocyte-specific SMOC-1 deletion increases cardiac rupture incidence and mortality post-AMI, while overexpression reduces rupture rates.
– SMOC-1 binds transforming growth factor β receptor 1 (TGF-βR1) and recruits glutamyl-prolyl-tRNA synthetase (EPRS) to activate Smad signaling, driving fibrosis.
