Abstract
In response to hypertension, the heart manifests robust hypertrophic growth, which offsets load-induced elevations in wall stress. If sustained, this hypertrophic response is a major risk factor for systolic dysfunction and heart failure. Extensive research efforts have focused on the progression from hypertrophy to failure; however, precise understanding of underlying mechanisms remains elusive. Recently, autophagy, a process of cellular cannibalization, has been implicated. Autophagy is activated during ventricular hypertrophy, serving to maintain cellular homeostasis. Excessive autophagy eliminates, however, essential cellular elements and possibly provokes cell death, which together contribute to hypertension-related heart disease.
Highlights
In response to hypertension, the heart manifests robust hypertrophic growth, which offsets load-induced elevations in wall stress
Recent studies highlight an important association between cardiovascular event rates and pre-hypertension, a state affecting Ͼ30% of the American population and defined as a systolic blood pressure between 120 and 139 mm Hg and/or a diastolic blood pressure between 80 and 89 mm Hg [3, 4]
Matsui et al [32] reported dramatic up-regulation of autophagosome formation 30 min after ischemia-inducing surgery. These results strongly suggest that autophagy is activated by myocardial ischemia
Summary
From the Departments of ‡Medicine (Cardiology) and §Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8573 leading cause of death worldwide [5]. The heart manifests robust hypertrophic growth, which offsets load-induced elevations in wall stress. If sustained, this hypertrophic response is a major risk factor for systolic dysfunction and heart failure. Essential cellular elements and possibly provokes cell death, which together contribute to hypertension-related heart disease. 2 The abbreviations used are: CVD, cardiovascular disease; LVH, left ventricular hypertrophy; TOR, target of rapamycin; mTOR, mammalian TOR; PI3K, Mechanisms of Remodeling in Hypertensive Heart Disease. Under conditions of stress, such as starvation and hypoxia, autophagy is activated, promoting cell survival by releasing energy substrates via degradation of cellular constituents and by eliminating defective or damaged organelles [19]. Working in concert, two kinase systems (ATG1-ATG13 and class III PI3K), two ubiquitin-like systems (ATG5-ATG12 and LC3-II-PE), and a retrieval/maturation system complete the autophagy flux pathway
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