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Article Addendum
Myocyte Autophagy in Heart Disease: Friend or Foe?
Beverly A. Rothermel and Joseph A. Hill
volume 3 | issue 6
November/December 2007Pages: 632 - 634
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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 Stress
H. Zhu, P. Tannous, J.L. Johnstone, Y. Kong, J.M. Shelton, J.A. Richardson, V. Le, B. Levine, B.A. Rothermel and J.A. Hill
J Clin Invest 2007;117:1782-93
Authors
Beverly A. Rothermel
University of Texas Southwestern Medical Center
Joseph A. Hill
University of Texas Southwestern Medical Center
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.