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      Autophagy and Mitophagy in Cardiovascular Disease.

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          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.

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          Author and article information

          Journal
          Circ. Res.
          Circulation research
          Ovid Technologies (Wolters Kluwer Health)
          1524-4571
          0009-7330
          May 26 2017
          : 120
          : 11
          Affiliations
          [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 George Pompidou, AP-HP, Paris, France (G.K.); Karolinska Institute, Department of Women's and Children's Health, Karolinska University Hospital, Stockholm, Sweden (G.K.); and Department of Radiation Oncology, Weill Cornell Medical College, New York, NY (L.G.).
          [2 ] 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 George Pompidou, AP-HP, Paris, France (G.K.); Karolinska Institute, Department of Women's and Children's Health, Karolinska University Hospital, Stockholm, Sweden (G.K.); and Department of Radiation Oncology, Weill Cornell Medical College, New York, NY (L.G.). kroemer@orange.fr deadoc@vodafone.it.
          Article
          CIRCRESAHA.117.311082
          10.1161/CIRCRESAHA.117.311082
          28546358
          bc67d4bd-0782-43d5-a7f6-546f822d00fe
          History

          apoptosis,atherosclerosis,endothelial cells,inflammation,necrosis

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