Nitric oxide, cell death, and heart failure.
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.
Oyama
Jun-ichi
J
Cardiovascular Division, Brigham and Women's Hospital, Boston, MA, USA.
Frantz
Stefan
S
Blais
Charles
C
Kelly
Ralph A
RA
Bourcier
Todd
T
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
D009569:Nitric Oxide