Abstract
Much 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).
| Original language | English |
|---|---|
| Pages (from-to) | 2751-2753 |
| Number of pages | 3 |
| Journal | Journal of Clinical Investigation |
| Volume | 117 |
| Issue number | 10 |
| DOIs | |
| State | Published - Oct 1 2007 |
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