Vascular access is the lifeblood of hemodialysis patients. Vascular remodeling develops after establishment of autogenous arteriovenous fistula (AVF), but some patients may have AVF stenosis in the vascular remodeling process, which then leads to access dysfunction and thus inadequate dialysis or failure in dialysis. Studies on the mechanism indicate that intimal hyperplasia is one of main pathological factors for AVF stenosis, while inflammation, uremia, hypoxia, shear stress and thrombus are the biological mechanism for intimal hyperplasia. In this paper, we reviewed the cell sources of intimal hyperplasia and the effects of inflammatory responses, inflammatory mediators and oxidative stress under different shear stresses produced by hemodynamic changes on intimal hyperplasia, and expected to bring forward new targets for the treatment of intimal hyperplasia.