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Circulation Research. 2000;87:184-188

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(Circulation Research. 2000;87:184.)
© 2000 American Heart Association, Inc.


Review

Vascular Cell Apoptosis in Remodeling, Restenosis, and Plaque Rupture

Kenneth Walsh, Roy C. Smith, Hyo-Soo Kim

From the Divisions of Cardiovascular Research and Vascular Medicine, St. Elizabeth’s Medical Center, and the Program in Cell, Molecular and Developmental Biology, Sackler School of Biomedical Studies, Tufts University School of Medicine, Boston, Mass.

Correspondence to Dr Kenneth Walsh, Division of Cardiovascular Research, St. Elizabeth’s Medical Center, 736 Cambridge St, Boston, MA 02135. E-mail kwalsh@world.std.com or kwalsh@opal.tufts.edu


Key Words: remodeling • atherosclerosis • restenosis • apoptosis


*    Introduction
 
This Review is part of a thematic series on Apoptosis in the Cardiovascular System, which includes the following articles: Apoptosis and Heart Failure: A Critical Review of the Literature

Vascular Cell Apoptosis in Remodeling, Restenosis, and Plaque Rupture

Apoptosis During Cardiovascular Development Myocyte Apoptosis in Ischemic Heart Disease Endothelial Cell Apoptosis in Angiogenesis and Vessel RegressionRichard Kitsis, Guest Editor

Apoptotic death of vascular cells is a prominent feature of blood vessel remodeling that occurs during normal development and fibroproliferative disorders of the vessel wall. This review summarizes a large number of studies that have provided evidence for apoptotic cell death in the vasculature. We also describe reports that shed light on the molecular mechanisms that may control this process. Finally, we highlight the relatively small number of studies that suggest a function for vascular cell apoptosis in controlling the morphology and cellular composition of the blood vessel wall.


*    Vascular Cell Apoptosis During Development and Flow-Induced Vessel Remodeling
 
A number of studies have demonstrated apoptotic death of vascular cells in vessels that remodel postnatally. Regionalized apoptosis has been found in vascular smooth muscle cells (VSMCs) during the regression and closure of the human ductus arteriosus before birth1 and in VSMCs and endothelial cells of the arteries and veins of the umbilical cord, which are subject to dramatic hemodynamic changes at birth.2 Evidence of VSMC apoptosis in the human neonate has also been found at the branch points of the great arteries arising from the aortic arch when they are exposed to a disturbed blood flow, whereas VSMC apoptosis . . . [Full Text of this Article]




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