title: Boosting autophagy in the diabetic heart: a translational perspective.
abstract: Diabetes, obesity, and dyslipidemia are main risk factors that promote the development of cardiovascular diseases. These metabolic abnormalities are frequently found to be associated together in a highly morbid clinical condition called metabolic syndrome. Metabolic derangements promote endothelial dysfunction, atherosclerotic plaque formation and rupture, cardiac remodeling and dysfunction. This evidence strongly encourages the elucidation of the mechanisms through which obesity, diabetes, and metabolic syndrome induce cellular abnormalities and dysfunction in order to discover new therapeutic targets and strategies for their prevention and treatment. Numerous studies employing both dietary and genetic animal models of obesity and diabetes have demonstrated that autophagy, an intracellular system for protein degradation, is impaired in the heart under these conditions. This suggests that autophagy reactivation may represent a future potential therapeutic intervention to reduce cardiac maladaptive alterations in patients with metabolic derangements. In fact, autophagy is a critical mechanism to preserve cellular homeostasis and survival. In addition, the physiological activation of autophagy protects the heart during stress, such as acute ischemia, starvation, chronic myocardial infarction, pressure overload, and proteotoxic stress. All these aspects will be discussed in our review article together with the potential ways to reactivate autophagy in the context of obesity, metabolic syndrome, and diabetes.
authors.affiliation: 1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
authors.forename: Sebastiano
authors.initials: S
authors.lastname: Sciarretta
authors.affiliation: 1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
authors.forename: V Subbarao
authors.initials: VS
authors.lastname: Boppana
authors.affiliation: 1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
authors.forename: Mahaa
authors.initials: M
authors.lastname: Umapathi
authors.affiliation: 1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
authors.forename: Giacomo
authors.initials: G
authors.lastname: Frati
authors.affiliation: 1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
authors.forename: Junichi
authors.initials: J
authors.lastname: Sadoshima
keywords: Autophagy; diabetes; heart; metabolic syndrome; obesity