title: Myocyte autophagy in heart disease: friend or foe?
abstract: In the setting of hemodynamic stress, such as occurs in hypertension or following myocardial infarction, the heart undergoes a compensatory hypertrophic growth response. Left unchecked, this hypertrophic response triggers myocyte death, ventricular dilation, diminished contractile performance, and a clinical syndrome of heart failure. For some years, autophagy has been implicated in heart failure. More recently, mechanistic studies have emerged which provide new insights into the molecular underpinnings of hemodynamic stress-induced cardiomyocyte autophagy. Further, these studies have begun to provide clues as to whether cardiomyocyte autophagy is adaptive, mitigating disease pathogenesis, or maladaptive, contributing to disease progression. Here, we discuss recent studies that both answer some questions and pose new ones.
authors.affiliation: Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, Texas 75390-8573, USA.
authors.forename: Beverly A
authors.initials: BA
authors.lastname: Rothermel
authors.forename: Joseph A
authors.initials: JA
authors.lastname: Hill
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins; D001343:Autophagy / Q000502:physiology*; D000071186:Beclin-1; D006332:Cardiomegaly / Q000235:genetics / Q000473:pathology; D006333:Heart Failure / Q000503:physiopathology*; D051379:Mice; D008822:Mice, Transgenic; D032383:Myocytes, Cardiac / Q000166:cytology / Q000502:physiology*; D011506:Proteins / Q000235:genetics; D013314:Stress, Mechanical; D020257:Ventricular Remodeling / Q000235:genetics