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 oxyge...

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Bibliographic Details
Published in:Heart failure reviews 2002-10, Vol.7 (4), p.327-334
Main Authors: Oyama, Jun-ichi, Frantz, Stefan, Blais, Jr, Charles, Kelly, Ralph A, Bourcier, Todd
Format: Article
Language:English
Subjects:
Apoptosis - physiology
Cell death
Genes, Tumor Suppressor
Heart Failure - metabolism
Heart Failure - physiopathology
Heart Transplantation - physiology
Humans
Myocardial Reperfusion Injury - metabolism
Myocardial Reperfusion Injury - physiopathology
Nitric Oxide - genetics
Nitric Oxide - metabolism
Ventricular Dysfunction, Left - metabolism
Ventricular Dysfunction, Left - physiopathology
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Summary: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.
ISSN:1382-4147
1573-7322
DOI:10.1023/A:1020758300499