BMAL1 attenuates myocardial infarction-induced fibrosis via suppressing p-SMAD3/SMAD3 in TGF-β1 pathway.

Cardiac function is markedly impaired as a result of myocardial fibrosis, a major pathological consequence that develops after myocardial infarction (MI). While BMAL1 (Brain and Muscle ARNT-like protein 1), a core circadian rhythm regulator, has been implicated in various cardiovascular pathologies, its role in post-MI cardiac fibrosis remains unclear. This study aimed to elucidate the role and underlying molecular mechanisms of BMAL1 in cardiac fibrosis. MI was induced in mice by permanent liga...