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Kathleen Martin

Martin Lab

Our studies in the Martin Lab are aimed at understanding the molecular mechanisms that regulate vascular smooth muscle cell (VSMC) phenotype. Mature SMC retain the ability to de-differentiate and re-enter the cell cycle. This is essential for such processes as angiogenesis, but also contributes to the pathogenesis of intimal hyperplasia. Intimal hyperplasia is a complication that contributes to the failure of angioplasty, stenting, and bypass surgery via restenosis, as well as long term failure of heart transplants due to diffuse graft arteriosclerosis.