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Cell Death in Cardiovascular Disease
Author(s) -
Martin R. Bennett
Publication year - 2011
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.111.239954
Subject(s) - programmed cell death , apoptosis , medicine , cause of death , necroptosis , disease , myocardial infarction , inflammation , proinflammatory cytokine , necrosis , thrombosis , pathology , biology , biochemistry
Cell death has been recognized in the cardiovascular system for centuries. In Virchow's 1858 lectures, he described atherosclerosis as producing new tissue, followed by cell death: “Thus, we have here an active process which really produces new tissues, but then hurries on to destruction in consequence of its own development.”1 Degraded and dying cells are found in both myocardial infarction and in atherosclerosis, and until the last 20 years were classified as necrosis. Death was considered a passive phenomenon due to ischemic or other insult, resulting in cell membrane dissolution and leakage of proinflammatory contents. The consequences of cell death resulted from loss of the function of the live cells and subsequent inflammation.This scenario changed with the description of apoptosis in the 1970s,2 and the subsequent detailed description of the mechanisms underlying this form of ‘programmed cell death.' The presence of apoptosis in atherosclerotic plaques has been confirmed by a number of studies.3–6 Apoptotic indices are low in early lesions (Stary grades I–III) but seen with increasing frequency as lesions develop, in both the necrotic core and fibrous cap. Apoptosis is …

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