TY - JOUR
T1 - Apoptosis and cardiomyopathy
AU - Narula, Jagat
AU - Kolodgie, Frank D.
AU - Virmani, Renu
PY - 2000
Y1 - 2000
N2 - Apoptosis is a form of cell death that has been described as distinct from necrotic cell death. It is believed to be genetically programmed and occurs as a physiologic process in various organ systems of body. Although it has been tacitly believed that apoptosis does not occur in the terminally differentiated adult heart muscle cells, studies in endomyocardial biopsies from patients with dilated and ischemic cardiomyopathy and in explanted hearts from patients with end-stage heart failure undergoing cardiac transplantation have demonstrated histochemical evidence of apoptosis. It has been proposed that ventricular dilatation and neurohormonal activation during heart failure lead to upregulation of transcription factors, induce myocyte hypertrophy, and prepare the cell for entry into the cell cycle. However, terminally differentiated myocytes cannot divide, and failing to divide they undergo apoptosis. Initiation of apoptosis is associated with activation of upstream cascade, including the release of cytochrome c from mitochondria to cytoplasm and the processing of proteolytic caspases. The activation of caspases leads to fragmentation of various cytoplasmic proteins, including contractile proteins. However, the nuclear fragmentation and condensation is completed only rarely. It is hypothesized that the release of cytochrome c from mitochondria and cytoplasmic protein loss in a living heart muscle cell should lead to systolic dysfunction. (C) 2000 Lippincott Williams and Wilkins, Inc.
AB - Apoptosis is a form of cell death that has been described as distinct from necrotic cell death. It is believed to be genetically programmed and occurs as a physiologic process in various organ systems of body. Although it has been tacitly believed that apoptosis does not occur in the terminally differentiated adult heart muscle cells, studies in endomyocardial biopsies from patients with dilated and ischemic cardiomyopathy and in explanted hearts from patients with end-stage heart failure undergoing cardiac transplantation have demonstrated histochemical evidence of apoptosis. It has been proposed that ventricular dilatation and neurohormonal activation during heart failure lead to upregulation of transcription factors, induce myocyte hypertrophy, and prepare the cell for entry into the cell cycle. However, terminally differentiated myocytes cannot divide, and failing to divide they undergo apoptosis. Initiation of apoptosis is associated with activation of upstream cascade, including the release of cytochrome c from mitochondria to cytoplasm and the processing of proteolytic caspases. The activation of caspases leads to fragmentation of various cytoplasmic proteins, including contractile proteins. However, the nuclear fragmentation and condensation is completed only rarely. It is hypothesized that the release of cytochrome c from mitochondria and cytoplasmic protein loss in a living heart muscle cell should lead to systolic dysfunction. (C) 2000 Lippincott Williams and Wilkins, Inc.
UR - http://www.scopus.com/inward/record.url?scp=0034116729&partnerID=8YFLogxK
U2 - 10.1097/00001573-200005000-00011
DO - 10.1097/00001573-200005000-00011
M3 - Review article
C2 - 10952426
AN - SCOPUS:0034116729
SN - 0268-4705
VL - 15
SP - 183
EP - 188
JO - Current Opinion in Cardiology
JF - Current Opinion in Cardiology
IS - 3
ER -