Brief Review |
From the Department of Internal Medicine and Cardiovascular Diseases (P.J.M.B., D.H., G.S., R.S.S., D.R.H., Jr, A.L.) and the Department of Biochemistry and Molecular Biology (R.D.S.), Mayo Clinic and Mayo Foundation, Rochester, Minn.
Correspondence to Amir Lerman, MD, Department of Internal Medicine and Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail lerman.amir{at}mayo.edu
AbstractApoptosis is an active form of cell death that is intricately regulated and distinct from necrosis. Data suggest that apoptosis may play a role in the pathophysiology of coronary atherosclerotic disease. Anatomic evidence of apoptosis has been observed in coronary atherosclerosis, restenosis, and transplant arteriopathy, accompanied by an increase in biochemical and genetic markers of apoptosis. Vasoactive substances such as nitric oxide and angiotensin II also regulate vascular smooth muscle cell apoptosis; vasodilating factors may induce apoptosis, whereas vasoconstricting factors may inhibit apoptosis. The aim of this article is to review key points regarding the detection of apoptosis, its regulation, and its possible role in the pathogenesis of coronary artery disease.
Key Words: apoptosis cell death atherosclerosis restenosis coronary disease
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