Apoptosis in the failing heart.
Apoptosis is a tightly regulated, energy-requiring process of programmed cell death. While necrosis is a form of cell death that results from acute cellular injury, apoptosis is controlled autodigestion of the cell that occurs through activation of endogenous proteases. This process results in the cleavage of chromatin into oligonucleosome-length DNA fragments and its multiples. This DNA fragmentation demonstrates a characteristic laddering pattern on DNA agarose gel electrophoresis. The heart undergoes extensive remodeling during embryogenesis wherein apoptosis significantly contributes to the development of the cardiac chambers and correct routing of the great vessels. Pathologic stimuli can also result in apoptosis and include ischemia, hypoxia, inflammation, cytokines, growth factors, and toxic agents. Better understanding of the molecular mechanisms responsible for regulating apoptosis in the failing myocardium may soon lead to strategies aimed at preventing further myocyte loss and enhancing myocyte replacement through regulated cell growth.
Narula
J
J
Massachusetts General Hospital, Boston, USA.
Hajjar
R J
RJ
Dec
G W
GW
D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D017209:Apoptosis; D016207:Cytokines / Q000502:physiology; D006333:Heart Failure / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009638:Norepinephrine / Q000502:physiology
D016207:Cytokines; D000804:Angiotensin II; D009638:Norepinephrine