Open AccessApoptosis in cardiac diseases: stress- and mitogen-activated signaling pathways
Author(s) -
Giora Feuerstein,
Peter R. Young
Publication year - 2000
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1016/s0008-6363(99)00372-7
Subject(s) - mapk/erk pathway , apoptosis , signal transduction , kinase , microbiology and biotechnology , mitogen activated protein kinase , p38 mitogen activated protein kinases , protein kinase a , biology , ceramide , angiotensin ii , ask1 , cardiac myocyte , myocyte , cancer research , medicine , receptor , mitogen activated protein kinase kinase , biochemistry
Apoptosis is a form of cell death that involves discrete genetic and molecular programs, de novo protein expression and a unique cellular phenotype. Evidence for the existence of apoptosis in the human heart has been reported in various cardiac diseases, including ischemic and non-ischemic heart failure, myocardial infarction and arrhythmias. Among the most potent stimuli that elicit cardiomyocyte apoptosis are: oxygen radicals (including NO), cytokines (FAS/TNF alpha-receptor signaling), stress conditions (chemical or physical, e.g., radiation), sphingolipid metabolites (ceramide) and autocoids, e.g., angiotensin II. Apoptosis of cardiac myocytes may contribute to progressive pump-failure, arrhythmias and cardiac remodeling. The recognition of numerous molecular targets associated with cardiomyocyte apoptosis may provide novel therapeutic strategies for diverse cardiac ailments, as recently suggested by pharmacologic studies in experimental animals. This review paper is aimed to highlight the role of protein kinase signaling pathways in apoptosis with special attention to the stress-activated protein kinases (SAPK) and mitogen-activated protein kinases (MAPK) systems.