Carboxy-terminal fragment of fibroblast growth factor 23 induces heart hypertrophy in sickle cell disease

摘要

Cardiac remodeling is frequently observed in patients with sickle cell disease (SCD), and contributes to cardiac dysfunction and premature death. 1,2 Cardiac dysfunction in SCD has been related to chronic anemia and low oxy- gen saturation. However, the mechanisms whereby they induce cardiac dysfunction are not completely under- stood and additional factors still have to be identified; a potential candidate is the fibroblast growth factor 23 (FGF23). FGF23 is secreted by bone cells and controls cal- citriol and serum phosphate concentrations by acting on the kidney, which is its main physiological target. 3 The intact form of FGF23 (iFGF23) is the only form that circu- lates under physiological conditions and mediates its physiological effects. iFGF23 can be cleaved in an N- and a C-terminal fragment and it is not certain whether these fragments have any biological effects.