title: This old heart: Cardiac aging and autophagy.
abstract: Autophagy, a cellular housekeeping process, is essential to maintain tissue homeostasis, particularly in long-lived cells such as cardiomyocytes. Autophagic activity declines with age and may explain many features of age-related cardiac dysfunction. In this review we summarize the current state of knowledge regarding age-related changes in autophagy in the heart. Recent findings from studies in human hearts are presented, including evidence that the autophagic response is intact in the aged human heart. Impaired autophagic clearance of protein aggregates or deteriorating mitochondria will have multiple consequences including increased arrhythmia risk, decreased contractile function, reduced tolerance to ischemic stress, and increased inflammation; thus autophagy represents a potentially important therapeutic target to mitigate the cardiac consequences of aging. This article is part of a Special Issue entitled CV Aging.
authors.affiliation: Donald P. Shiley BioScience Center, San Diego State University, San Diego, CA, USA.
authors.forename: Phyllis-Jean
authors.initials: PJ
authors.lastname: Linton
authors.affiliation: Donald P. Shiley BioScience Center, San Diego State University, San Diego, CA, USA.
authors.forename: Michael
authors.initials: M
authors.lastname: Gurney
authors.affiliation: Division of Geriatric Medicine, Oakwood Hospital, Dearborn, MI, USA; Department of Internal Medicine, Wayne State University School of Medicine, Detroit, MI, USA.
authors.forename: David
authors.initials: D
authors.lastname: Sengstock
authors.affiliation: Cardiovascular Research Institute, Departments of Surgery and Physiology, Wayne State University School of Medicine, Detroit, MI, USA; Heart Institute and Barbra Streisand Women's Heart Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
authors.forename: Robert M
authors.initials: RM
authors.lastname: Mentzer
authors.affiliation: Heart Institute and Barbra Streisand Women's Heart Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Roberta.Gottlieb@cshs.org.
authors.forename: Roberta A
authors.initials: RA
authors.lastname: Gottlieb
mesh_terms: D000375:Aging / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D001343:Autophagy / Q000235:genetics*; D005786:Gene Expression Regulation; D006706:Homeostasis; D006801:Humans; D008136:Longevity; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D011494:Protein Kinases / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D044767:Ubiquitin-Protein Ligases / Q000235:genetics / Q000378:metabolism; D000099202:PTEN-Induced Putative Kinase
chemical_list: D008869:Microtubule-Associated Proteins; D011494:Protein Kinases; D044767:Ubiquitin-Protein Ligases; D000099202:PTEN-Induced Putative Kinase; C477012:MAP1LC3A protein, human; C111567:parkin protein
keywords: Aging; Autophagy; Cardiac; Human studies; Inflammation