Restenosis following coronary angioplasty is thought to result from the migration and proliferation of medial smooth muscle cells (SMCs) into the intimal lesion. However, the factors responsible for the development of restenosis are still unknown. Experimental and clinical studies have shown that endothelial dysfunction is an early event preceding restenosis, and that subsequent activation of platelets and leukocytes on the injured arterial wall contributes to the migration and proliferation of SMCs. This review presents a critical discussion of evidence for and against a role for leukocytes, giving special consideration to neutrophils, and the leukocyte adhesion molecules in the development of intimal hyperplasia and restenosis.
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