Nitric oxide and angiogenesis

At cardiovascular level angiogenesis is sought for tissue reperfusion following ischemia and accelerates the healing process. Endothelial dysfunction and reduced production of nitric oxide (NO) cause cardiovascular diseases and the impairment to mount an adequate angiogenic response. We have contributed to demonstrate that NO directs endothelial cells in each step of angiogenesis. Peptides as substance P and bradykinin and vascular endothelial growth factor (VEGF) promote their effects by upregulating the NOS/cGMP pathway, which brings to the MAPK-dependent upregulation of fibroblast growth factor-2 (FGF-2). Experimental evidences indicate that by these molecular paths, new and consolidated pharmacological approaches increasing NO production in the endothelium induce endothelium re-growth and angiogenesis.