Autophagy and Mitophagy in Cardiovascular Disease

Author:

Bravo-San Pedro José Manuel1,Kroemer Guido1,Galluzzi Lorenzo1

Affiliation:

1. From the Université Paris Descartes/Paris V, Sorbonne Paris Cité, France (J.M.B.-S.P., G.K., L.G.); Université Pierre et Marie Curie/Paris VI, France (J.M.B.-S.P., G.K.); INSERM, U1138, Paris, France (J.M.B.-S.P., G.K.); Equipe 11 labellisée Ligue contre le Cancer, Centre de Recherche des Cordeliers, Paris, France (J.M.B.-S.P., G.K.); Metabolomics and Cell Biology Platforms, Gustave Roussy Comprehensive Cancer Institute, Villejuif, France (J.M.B.-S.P., G.K.); Pôle de Biologie, Hopitâl Européen...

Abstract

Autophagy contributes to the maintenance of intracellular homeostasis in most cells of cardiovascular origin, including cardiomyocytes, endothelial cells, and arterial smooth muscle cells. Mitophagy is an autophagic response that specifically targets damaged, and hence potentially cytotoxic, mitochondria. As these organelles occupy a critical position in the bioenergetics of the cardiovascular system, mitophagy is particularly important for cardiovascular homeostasis in health and disease. Consistent with this notion, genetic defects in autophagy or mitophagy have been shown to exacerbate the propensity of laboratory animals to spontaneously develop cardiodegenerative disorders. Moreover, pharmacological or genetic maneuvers that alter the autophagic or mitophagic flux have been shown to influence disease outcome in rodent models of several cardiovascular conditions, such as myocardial infarction, various types of cardiomyopathy, and atherosclerosis. In this review, we discuss the intimate connection between autophagy, mitophagy, and cardiovascular disorders.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

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