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Losing heart: the role of apoptosis in heart disease—a novel therapeutic target?
Author(s) -
Gill Catherine,
Mestril Ruben,
Samali Afshin
Publication year - 2002
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.01-0629com
Subject(s) - programmed cell death , apoptosis , microbiology and biotechnology , caspase , necrosis , signal transduction , biology , mechanism (biology) , cytochrome c , mitochondrion , medicine , cancer research , biochemistry , philosophy , epistemology
Cardiovascular disease is a leading cause of death worldwide. In recent years it has emerged that loss of myocardial cells may be a major pathogenic factor. Cell death can occur in a destructive, uncontrolled manner via necrosis or by a highly regulated programmed cell suicide mechanism termed apoptosis. As cell death in conditions such as heart failure and myocardial infarction does not always follow a typically apoptotic pathway, it remains to be established whether it occurs by apoptosis, necrosis, or a novel uncharacter‐ized mechanism combining aspects of both types of cell death. Apoptotic pathways have been well studied in nonmyocytes and it is thought that similar pathways exist in cardiomyocytes. These pathways include death initiated by ligation of membrane‐bound death receptors or death initiated by release of cytochrome c from mitochondria. Increasing evidence supports the existence of these pathways and their regulators in the heart. These regulators include inhibitors of caspases, which are the key enzymes of apoptosis, the Bcl‐2 family of proteins, growth factors, stress proteins, calcium, and oxidants. It is hoped that a better understanding of the pathways of apoptosis and their regulation may yield novel therapeutic targets for cardiovascular disease.—Gill, C., Mestril, R., Samali, A. Losing heart: the role of apoptosis in heart disease—a novel therapeutic target? FASEB J. 16, 135–146 (2002)