FGF23 and Cardiovascular Risk

Abstract

FGF23 is a protein secreted in the plasma by bone cells. In the kidney, FGF23 can activate an FGF receptor in the presence of its co-receptor αKlotho. FGF23 controls the renal phosphate reabsorption and calcitriol metabolism. When renal function declines, plasma FGF23 concentration raises and FGF23 can stimulate FGFRs in the absence of αKlotho. This induces cardiac hypertrophy, modifies cardiomyocyte contractility and increases the risk of arrhythmic events in cardiac cells. There is still no evidence that decreasing FGF23 concentration in patients on dialysis could improve their survival. In different cardiac disorders cardiomyocyte can produce FGF23, which can reveal a way of adaptation to the stress.