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Vascular Smooth Muscle Cell Migration: Current Research and Clinical Implications
A. I. Willis, MD
D. Pierre-Paul, MD
B. E. Sumpio, MD, PhD
Yale University School of Medicine, New Haven, CT and the VA Connecticut Healthcare System, West Haven, CT
V. Gahtan, MD
Yale University School of Medicine, New Haven, CT and the VA Connecticut Healthcare System, West Haven, CT; SUNY Upstate Medical University College of Medicine, Section of Vascular Surgery, 750 East Adams Street, Syracuse, NY 13210 gahtanv{at}upstate.edu
Atherosclerosis and intimal hyperplasia are major causes of morbidity and mortality. These processes develop secondary to endothelial injury due to multiple stimuli, including smoking, diabetes mellitus, hypertension, and hyperlipidemia. Once this injury occurs, an essential element in the development of both these processes is vascular smooth muscle cell (VSMC) migration. Understanding the mechanisms involved in VSMC migration and ultimately the development of strategies by which this process can be inhibited, has been a major focus of research. The authors present a review of the extracellular proteins (growth factors, extracellular matrix components, and cell surface receptors) and intracellular signaling pathways involved in VSMC migration, as well as potential therapeutic approaches to inhibit this process.
Vascular and Endovascular Surgery, Vol. 38, No. 1,
11-23 (2004)
DOI: 10.1177/153857440403800102

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