title: Mitochondrial aging and age-related dysfunction of mitochondria.
abstract: Age-related changes in mitochondria are associated with decline in mitochondrial function. With advanced age, mitochondrial DNA volume, integrity and functionality decrease due to accumulation of mutations and oxidative damage induced by reactive oxygen species (ROS). In aged subjects, mitochondria are characterized by impaired function such as lowered oxidative capacity, reduced oxidative phosphorylation, decreased ATP production, significant increase in ROS generation, and diminished antioxidant defense. Mitochondrial biogenesis declines with age due to alterations in mitochondrial dynamics and inhibition of mitophagy, an autophagy process that removes dysfunctional mitochondria. Age-dependent abnormalities in mitochondrial quality control further weaken and impair mitochondrial function. In aged tissues, enhanced mitochondria-mediated apoptosis contributes to an increase in the percentage of apoptotic cells. However, implementation of strategies such as caloric restriction and regular physical training may delay mitochondrial aging and attenuate the age-related phenotype in humans.
authors.affiliation: Department of Medical Nanobiotechnology, Pirogov Russian State Medical University, Moscow 117997, Russia.
authors.forename: Dimitry A
authors.initials: DA
authors.lastname: Chistiakov
authors.affiliation: Laboratory of Medical Genetics, Russian Cardiology Research and Production Complex, Moscow 121552, Russia ; Laboratory of Cellular Mechanisms of Atherogenesis, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia.
authors.forename: Igor A
authors.initials: IA
authors.lastname: Sobenin
authors.affiliation: Biological Faculty, N.P. Ogaryov Mordovian State University, Saransk 430005, Russia.
authors.forename: Victor V
authors.initials: VV
authors.lastname: Revin
authors.affiliation: Laboratory of Cellular Mechanisms of Atherogenesis, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia ; Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 143025, Russia.
authors.forename: Alexander N
authors.initials: AN
authors.lastname: Orekhov
authors.affiliation: Biological Faculty, N.P. Ogaryov Mordovian State University, Saransk 430005, Russia ; Faculty of Medicine, University of New South Wales, Sydney, NSW 2052, Australia ; School of Medicine, University of Western Sydney, Campbelltown, NSW 2560, Australia.
authors.forename: Yuri V
authors.initials: YV
authors.lastname: Bobryshev
mesh_terms: D000375:Aging / Q000473:pathology*; D000818:Animals; D016922:Cellular Senescence; D004272:DNA, Mitochondrial / Q000235:genetics; D006801:Humans; D008928:Mitochondria / Q000235:genetics / Q000473:pathology*; D063154:Mitochondrial Dynamics / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D004272:DNA, Mitochondrial; D017382:Reactive Oxygen Species