Exercise-mediated regulation of autophagy in the cardiovascular system

Abstract

Cardiovascular disease is the leading cause of human death worldwide. Autophagy is an evolutionarily conserved degradation pathway, which is a highly conserved cellular degradation process in which lysosomes decompose their own organelles and recycle the resulting macromolecules. Autophagy is critical in maintaining cardiovascular homeostasis and function, and excessive or insufficient autophagy or autophagic flux can lead to cardiovascular disease. Enormous evidence indicates that exercise training plays a beneficial role in the prevention and treatment of cardiovascular diseases. The regulation of autophagy during exercise is a bidirectional process. For cardiovascular disease caused by either insufficient or excessive autophagy, exercise training restores normal autophagy function and delays the progression of cardiovascular disease. An in-depth exploration and discussion of exercise-mediated regulation of autophagy in the cardiovascular system can broaden our view about the prevention of various autophagy-related diseases through exercise training. In this article, we review autophagy and its related signaling pathways, as well as autophagy-dependent beneficial effects of exercise in cardiovascular system.

Keywords: Autophagy; Cardiovascular diseases; Exercise.

Graphical abstract

Fig. 1

Mechanisms involved in autophagy process. After inhibition of the mTOR or activation of the AMPK signaling pathway, the autophagy process is activated. AMPK = adenosine monophosphate-activated protein kinase; ATP = adenosine triphosphate; mTOR = mammalian target of rapamycin; PI3K = phosphatidylinositol-3-kinase; ULK1 = Unc-51 like autophagy activating kinase 1; Vps = vacuolar protein sorting.

Fig. 2

The cardioprotection effects of exercise via modulation of autophagy. Exercise-mediated bidirectional regulation of autophagy can prevent cardiovascular diseases.