Abstract

Follistatin-like 1 (FSTL1) is a key factor in maintaining cardiac growth and development. It can be activated by exercise training and has a dual role in promoting cardiomyocyte proliferation and fibrosis, but its underlying mechanism is not fully understood. To elucidate the dual mechanism and target of FSTL1 regulating of cardiomyocyte proliferation and myocardial fibrosis, and the mechanism by which exercise-regulated FSTL1 improves cardiovascular disease, we explored the signal transduction pathway of FSTL1 promoting cardiomyocyte proliferation and fibrosis, and compared the effects of different modes of exercise on the dual role of FSTL1. We believe that the dual role of promoting cardiomyocyte proliferation and fibrosis may be related to the ratio of cardiomyocyte and myocardial interstitial cell proliferation, different stages of the disease, different degrees of fibrosis, immune repair process, and transforming growth factor-β activation. Compared with long-term excessive endurance exercise, moderate resistance exercise can activate cardiomyocyte proliferation pathway through FSTL1, which is one of the effective ways to prevent cardiovascular disease.

Full Text
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