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- W1987443589 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 questions and pose new ones.Addendum to:Cardiac Autophagy is a Maladaptive Response to Hemodynamic StressH. Zhu, P. Tannous, J.L. Johnstone, Y. Kong, J.M. Shelton, J.A. Richardson, V. Le, B. Levine, B.A. Rothermel and J.A. HillJ Clin Invest 2007;117:1782-93" @default.
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- W1987443589 date "2007-11-26" @default.
- W1987443589 modified "2023-10-01" @default.
- W1987443589 title "Myocyte Autophagy in Heart Disease: Friend or Foe?" @default.
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- W1987443589 doi "https://doi.org/10.4161/auto.4913" @default.
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