Wall shear stress promotes intimal hyperplasia through the paracrine H2O2-mediated NOX-AKT-SVV axis

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Abstract

Aims:

Oscillatory wall shear stress (WSS)-linked oxidative stress promotes intimal hyperplasia (IH) development, but the underlying mechanisms are not completely understood.

Materials and methods:

We used an in vivo rabbit carotid arterial stenosis model representing different levels of WSS and found that WSS was increased at 1month 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 findings:

Our in vitro study suggested that H2O2 promoted proliferation and migration while suppressing apoptosis in cultured human umbilical vascular endothelial cells.

Significance:

We 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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