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 (US) |
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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 |
ASJC Scopus subject areas
- Medicine(all)