Type, intensity, and duration of exercise in regulating cardiac remodelling via FSTL1

Abstract Cardiovascular disease (CVD) is one of the major health issues and world's first leading cause of death. An increasing number of premature mortalities in CVD has become a current concern among young adults mostly due to the sedentary lifestyle of lacking exercise. Regular exercise is well-known for its beneficial adaptations in the cardiovascular system by inducing secretion of follistatin-like 1 (FSTL1). This review aims to investigate the potential mechanisms of FSTL1 to promote cardiac remodelling especially in inducing cardiomyocytes (CMs) proliferation based on types, intensities, and durations of exercise. Some molecular mechanisms, such as cytokines, microRNA (miR), transcription factors, and other signalling pathways are implied to generate cardiovascular remodelling. Thus, exercise-induced FSTL1 and its downstream, phosphatidylinositol-3-kinase-protein kinase B-mammalian target or rapamycin (PI3K-Akt-mTOR) signalling pathway are a promising approach to maintaining, improving, and attenuating cardiovascular function in healthy, at-risk, and/or sick people. Nevertheless, further study is needed to verify these specific mechanisms and contribute more clinical evidence.