Osteopontin: an emerging therapeutic target in uraemic vascular disease

This editorial refers to ‘Osteopontin deficiency dampens the pro-atherogenic effect of uraemia’ by T.X. Pedersen et al. , pp. 352–359, this issue. The incidence of cardiovascular disease remains high in the population with renal failure and constitutes the leading cause of morbidity and mortality in these patients. According to the U.S. Renal Data System 2011 Annual Data Report, the rate of death among dialysis patients attributable to cardiovascular disease was 40% and 5% to acute myocardial infarction.1 However, the mechanisms by which renal failure accelerates development of vascular disease and magnifies cardiovascular morbidity and mortality remain elusive.As a common component in development of atherosclerosis, calcification characterizes vasculopathy, contributes to plaque rupture and thrombosis, and predicts high mortality in hemodialysis patients.2 In addition to traditional risk factors, this complication is associated with non-traditional factors such as elevated serum phosphorus and serum calcium × phosphorus product in uraemia.3 However, recent evidence suggests that the mechanism underpinning vascular calcification in uraemia is more than passive metastatic calcification, but an active cell-mediated process. Furthermore, osteopontin (OPN) has emerged as a key regulator in development of atherosclerosis-associated vasculopathy.OPN, a small integrin-binding ligand, N -linked (SIBLING) glycoprotein first identified in 1986 as …