Abstract
AimsOscillatory wall shear stress (WSS)-linked oxidative stress promotes intimal hyperplasia (IH) development, but the underlying mechanisms are not completely understood. Materials and methodsWe used an in vivo rabbit carotid arterial stenosis model representing different levels of WSS and found that WSS was increased at 1 month with 50% stenosis and was accompanied by VSMCs proliferation and interstitial collagen accumulation. Increased WSS promoted the expression of NOX, AKT, and survivin (SVV) and the proliferation/migration of VSMCs and reduced apoptosis. Key findingsOur in vitro study suggested that H2O2 promoted proliferation and migration while suppressing apoptosis in cultured human umbilical vascular endothelial cells. SignificanceWe demonstrated that the elevation of WSS promotes VSMC proliferation and migration through the H2O2-mediated NOX-AKT-SVV axis, thereby accelerating IH development.
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