title: New insights into the role of mitochondrial dynamics and autophagy during oxidative stress and aging in the heart.
abstract: The heart is highly sensitive to the aging process. In the elderly, the heart tends to become hypertrophic and fibrotic. Stiffness increases with ensuing systolic and diastolic dysfunction. Aging also affects the cardiac response to stress. At the molecular level, the aging process is associated with accumulation of damaged proteins and organelles, partially due to defects in protein quality control systems. The accumulation of dysfunctional and abnormal mitochondria is an important pathophysiological feature of the aging process, which is associated with excessive production of reactive oxygen species. Mitochondrial fusion and fission and mitochondrial autophagy are crucial mechanisms for maintaining mitochondrial function and preserving energy production. In particular, mitochondrial fission allows for selective segregation of damaged mitochondria, which are afterward eliminated by autophagy. Unfortunately, recent evidence indicates that mitochondrial dynamics and autophagy are progressively impaired over time, contributing to the aging process. This suggests that restoration of these mechanisms could delay organ senescence and prevent age-associated cardiac diseases. Here, we discuss the current understanding of the close relationship between mitochondrial dynamics, mitophagy, oxidative stress, and aging, with a particular focus on the heart.
authors.affiliation: Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, 185 South Orange Avenue, Medical Science Building G-609, Newark, NJ 07103, USA.
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Ikeda
authors.affiliation: Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, 185 South Orange Avenue, Medical Science Building G-609, Newark, NJ 07103, USA ; IRCCS Neuromed, Via Atinense 18, 86077 Pozzilli, Italy.
authors.forename: Sebastiano
authors.initials: S
authors.lastname: Sciarretta
authors.affiliation: Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, 185 South Orange Avenue, Medical Science Building G-609, Newark, NJ 07103, USA.
authors.forename: Narayani
authors.identifier: 0000-0003-3950-564X
authors.initials: N
authors.lastname: Nagarajan
authors.affiliation: IRCCS Neuromed, Via Atinense 18, 86077 Pozzilli, Italy ; Division of Cardiology, Department of Clinical and Molecular Medicine, Faculty of Medicine and Psychology, Sapienza University, Via di Grottarossa 1035-1039, 00189 Rome, Italy.
authors.forename: Speranza
authors.initials: S
authors.lastname: Rubattu
authors.affiliation: IRCCS Neuromed, Via Atinense 18, 86077 Pozzilli, Italy ; Division of Cardiology, Department of Clinical and Molecular Medicine, Faculty of Medicine and Psychology, Sapienza University, Via di Grottarossa 1035-1039, 00189 Rome, Italy.
authors.forename: Massimo
authors.initials: M
authors.lastname: Volpe
authors.affiliation: IRCCS Neuromed, Via Atinense 18, 86077 Pozzilli, Italy ; Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University, Corso della Repubblica 79, 04100 Latina, Italy.
authors.forename: Giacomo
authors.initials: G
authors.lastname: Frati
authors.affiliation: Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, 185 South Orange Avenue, Medical Science Building G-609, Newark, NJ 07103, USA.
authors.forename: Junichi
authors.initials: J
authors.lastname: Sadoshima
mesh_terms: D000375:Aging; D000818:Animals; D001343:Autophagy; D006321:Heart / Q000502:physiology*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D063154:Mitochondrial Dynamics; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species