Abstract
Introduction: TGF-β has been shown to be a critical element in the development of neointimal hyperplasia. We have previously found that stimulation of the TGF-β/Smad3 pathway induces smooth muscle cell (SMC) proliferation, thus enhancing neointimal formation. In the current study, we hypothesize that blockade of TGF-β and Smad3 signaling, through overexpression of the endogenous inhibitor Smad7, decreases neointimal hyperplasia by inhibiting cell proliferation. Methods: Male Sprague-Dawley rats underwent left carotid balloon injury followed by intra-arterial dwell with adenoviral vectors expressing Smad7 or LacZ (AdSmad7 or AdLacZ).
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