Abstract
Heart failure represents the terminal stage of cardiovascular disease, with cardiac remodeling as a key pathological feature. As a core circadian clock gene, brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1 (BMAL1) not only regulates circadian rhythms but also plays a critical role in cardiac remodeling. Studies have shown that BMAL1 deficiency leads to myocardial metabolic dysfunction, cardiomyocyte hypertrophy, activation of the inflammatory response, fibrosis, and impaired cardiac function, thereby promoting the onset and progression of heart failure. This review systematically summarizes the mechanisms by which BMAL1 influences heart failure, with a focus on its regulatory roles in metabolism, inflammation, and fibrosis. Furthermore, we explore clinical translational potential and future prospects of correcting circadian rhythm disruption and chronotherapy in heart failure, aiming to provide new insights and directions for its treatment.