title: Nipping at cardiac remodeling.
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.
authors.affiliation: Department of Medicine, Cardiovascular Research Center, Albert Einstein College of Medicine, New York, New York, USA.
authors.forename: Russell S
authors.initials: RS
authors.lastname: Whelan
authors.forename: Kartik
authors.initials: K
authors.lastname: Mani
authors.forename: Richard N
authors.initials: RN
authors.lastname: Kitsis
mesh_terms: 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
chemical_list: C090121:BNIP3 protein, human; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins