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Welcome to the Martin Lab!


Our overall goal is to understand how regulation of the muscular layer of blood vessels contributes to normal vessel function and to cardiovascular disease. Hyperproliferation or dysfunction in vascular smooth muscle cells contributes to atherosclerosis, hypertension, organ transplant failure, and failure of revascularization therapies such as balloon angioplasty or bypass surgery. By understanding the regulatory mechanisms of vascular smooth muscle, we aim to develop new therapies for treatment and prevention of cardiovascular diseases.

Key areas of interest: Vascular smooth muscle; Differentiation; Signal transduction; Transcription; Epigenetics

Disease models: Atherosclerosis, Intimal Hyperplasia, Transplant Vasculopathy, Obesity and Diabetes

Our studies aim to understand the molecular mechanisms that regulate vascular smooth muscle cell (SMC) phenotypic plasticity. 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 atherosclerosis, intimal hyperplasia, and restenosis.