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Abnormal proliferation of vascular smooth muscle cells (SMCs) is thought to contribute to neointimal thickening during spontaneous atherosclerosis and vessel renarrowing (restenosis) after angioplasty. This review will focus on the mechanisms underlying cell-cycle control in SMCs and its implication in atherosclerosis and restenosis. Therapeutic approaches that targeted specific cell-cycle control genes or growth regulatory molecules which effectively inhibited neointimal lesion formation will also be discussed.
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Vicente Andrés (1998) studied this question.
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