Fibroblast growth factor (FGF) 23 and FGF receptor 4 induced cardiac mitochondrial dysfunction as a new target in CKD?

Abstract

Chronic kidney disease is associated with excessive cardiovascular mortality, which is promoted by the phosphaturic hormone fibroblast growth factor 23 (FGF23). Increased FGF23 levels result in left ventricular hypertrophy via activation of the FGF receptor 4 activation. Fuchs et al. now demonstrate, using bioengineered cardiobundles, neonatal rat ventricular myocytes, and mice with chronic kidney disease, that FGF23–FGF receptor 4 activation is a potential mechanism of cardiac mitochondrial dysfunction and metabolic remodeling as early complications of chronic kidney disease, preceding structural cardiac changes.