Russell S. Whelan, Kartik Mani, Richard N. Kitsis
J Clin Invest.
2007;
117(10):2751–2753
doi:10.1172/JCI33706
This article Copyright © 2007, The American Society for Clinical Investigation
Abstract
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uch of the mortality following myocardial infarction results from remodeling of the heart after the acute ischemic event. Cardiomyocyte apoptosis has been thought to play a key role in this remodeling process. In this issue of the JCI, Diwan and colleagues present evidence that Bnip3, a proapoptotic Bcl2 family protein, mediates cardiac enlargement, reshaping, and dysfunction in mice without influencing infarct size (see the related article beginning on page 2825).
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