title: Nitric oxide, cell death, and heart failure.
abstract: Strong evidence links cardiomyocyte loss to the pathology of some forms of heart failure. Both necrotic and apoptotic modes of cell death have been invoked as the mechanism underlying progressive cardiomyocyte dropout. Nitric oxide (NO) has received particular attention as a candidate reactive oxygen intermediate that influences not only cardiac function, but also cell death elicited by both apoptotic and necrotic mechanisms. NO is produced by resident cardiac cells under stress, and is produced in large quantities by activated immune cells that infiltrate the injured heart. A review of the literature, however, reveals that the actions of NO on apoptotic cell death are complex, especially in the context of heart disease, and that the practical contribution of NO to cell death in heart disease is yet to be defined.
authors.affiliation: Cardiovascular Division, Brigham and Women's Hospital, Boston, MA, USA.
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Oyama
authors.forename: Stefan
authors.initials: S
authors.lastname: Frantz
authors.forename: Charles
authors.initials: C
authors.lastname: Blais
authors.forename: Ralph A
authors.initials: RA
authors.lastname: Kelly
authors.forename: Todd
authors.initials: T
authors.lastname: Bourcier
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D016147:Genes, Tumor Suppressor; D006333:Heart Failure / Q000378:metabolism* / Q000503:physiopathology; D016027:Heart Transplantation / Q000502:physiology; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D009569:Nitric Oxide / Q000235:genetics / Q000378:metabolism*; D018487:Ventricular Dysfunction, Left / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D009569:Nitric Oxide