作者: Juan Rafael Muñoz-Castañeda , Cristian Rodelo-Haad , Maria Victoria Pendon-Ruiz de Mier , Alejandro Martin-Malo , Rafael Santamaria
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摘要: Fibroblast Growth Factor 23 (FGF23) and Klotho play an essential role in the regulation of mineral metabolism, both are altered as a consequence renal failure. FGF23 increases to augment phosphaturia, which prevents phosphate accumulation at early stages chronic kidney disease (CKD). This effect requires presence tubules. However, expression is reduced soon function starting fail generate state resistance. Changes these proteins directly affect other metabolism parameters; they may can produce damage organs such bone, heart, or vessels. Some mechanisms responsible for changes levels related modifications Wnt signaling. review examines link between FGF23/Klotho Wnt/β-catenin different organs: kidney, bone. Activation canonical signaling produces vice versa; therefore, this pathway emerges potential therapeutic target that help prevent CKD-associated complications.