Nipping at cardiac remodeling.
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.
Whelan
Russell S
RS
Department of Medicine, Cardiovascular Research Center, Albert Einstein College of Medicine, New York, New York, USA.
Mani
Kartik
K
Kitsis
Richard N
RN
D000818:Animals; D017209:Apoptosis; D002303:Cardiac Output, Low / Q000209:etiology / Q000378:metabolism* / Q000401:mortality; D006801:Humans; D008565:Membrane Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051379:Mice; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology*; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D020257:Ventricular Remodeling
C090121:BNIP3 protein, human; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins