title: Mitochondrial dysfunction in cardiac aging.
abstract: Cardiovascular diseases are the leading cause of death in most developed nations. While it has received the least public attention, aging is the dominant risk factor for developing cardiovascular diseases, as the prevalence of cardiovascular diseases increases dramatically with increasing age. Cardiac aging is an intrinsic process that results in impaired cardiac function, along with cellular and molecular changes. Mitochondria play a great role in these processes, as cardiac function is an energetically demanding process. In this review, we examine mitochondrial dysfunction in cardiac aging. Recent research has demonstrated that mitochondrial dysfunction can disrupt morphology, signaling pathways, and protein interactions; conversely, mitochondrial homeostasis is maintained by mechanisms that include fission/fusion, autophagy, and unfolded protein responses. Finally, we describe some of the recent findings in mitochondrial targeted treatments to help meet the challenges of mitochondrial dysfunction in aging.
authors.affiliation: University of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: uw.tocchi@gmail.com.
authors.forename: Autumn
authors.initials: A
authors.lastname: Tocchi
authors.affiliation: University of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: equarles@gmail.com.
authors.forename: Ellen K
authors.initials: EK
authors.lastname: Quarles
authors.affiliation: University of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: nbasisty@uw.edu.
authors.forename: Nathan
authors.initials: N
authors.lastname: Basisty
authors.affiliation: University of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: mlemuel@uw.edu.
authors.forename: Lemuel
authors.initials: L
authors.lastname: Gitari
authors.affiliation: University of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: petersr@u.washington.edu.
authors.forename: Peter S
authors.initials: PS
authors.lastname: Rabinovitch
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D001343:Autophagy; D031204:Caloric Restriction; D002308:Cardiolipins / Q000502:physiology; D004249:DNA Damage; D004734:Energy Metabolism; D006321:Heart / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D008928:Mitochondria / Q000473:pathology / Q000502:physiology*; D011506:Proteins / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D056811:Unfolded Protein Response
chemical_list: D002308:Cardiolipins; D011506:Proteins
keywords: Aging; Heart; Mitochondrial dysfunction; Mitostasis