C-reactive protein incites atherosclerosis.

Accumulating evidence suggests that C-reactive protein (CRP) levels are a robust and independent predictor of future cardiovascular events. By the same token, increasing data point toward a proatherogenic role of CRP. The present review outlines some of the emerging data that suggest that CRP may directly promote the development of endothelial dysfunction, by affecting endothelium-derived contracting and relaxing factors such as nitric oxide, endothelin, angiotensin and interleukin-6. More recently, CRP has been demonstrated to inhibit the survival and differentiation of bone marrow-derived endothelial progenitor cells, which play a key role in postnatal neovascularization.