Non-Classical Effects of FGF23: Molecular and Clinical Features
Metadatos
Mostrar el registro completo del ítemAutor
Martínez Heredia, Luis; Canelo-Moreno, Juan Manuel; García Fontana, Beatriz; Muñoz Torres, Manuel EduardoEditorial
MDPI
Materia
FGF23 Klotho Calcineurin pathway
Fecha
2024-04-30Referencia bibliográfica
Martínez-Heredia, L.; Canelo-Moreno, J.M.; García-Fontana, B.; Muñoz-Torres, M. Non-Classical Effects of FGF23: Molecular and Clinical Features. Int. J. Mol. Sci. 2024, 25, 4875. [https://doi.org/10.3390/ijms25094875]
Patrocinador
Institute of Health Carlos III grant (PI22/00726) co-funded by the European Regional Development Fund (FEDER); LM-H and BG-F are funded by CIBER of Frailty and Healthy Aging (CIBERFES;CB16/10/00475) and by Institute of Health Carlos III grant (CP22/00022) respectively.Resumen
This article reviews the role of fibroblast growth factor 23 (FGF23) protein in phosphate
metabolism, highlighting its regulation of vitamin D, parathyroid hormone, and bone metabolism.
Although it was traditionally thought that phosphate–calcium homeostasis was controlled exclusively
by parathyroid hormone (PTH) and calcitriol, pathophysiological studies revealed the influence
of FGF23. This protein, expressed mainly in bone, inhibits the renal reabsorption of phosphate
and calcitriol formation, mediated by the α-klotho co-receptor. In addition to its role in phosphate
metabolism, FGF23 exhibits pleiotropic effects in non-renal systems such as the cardiovascular,
immune, and metabolic systems, including the regulation of gene expression and cardiac fibrosis.
Although it has been proposed as a biomarker and therapeutic target, the inhibition of FGF23 poses
challenges due to its potential side effects. However, the approval of drugs such as burosumab
represents a milestone in the treatment of FGF23-related diseases.