Hospital Universitario Reina Sofía, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Universidad de Córdoba, Córdoba, Spain.
Adv Ther. 2020 May;37(Suppl 2):73-79. doi: 10.1007/s12325-019-01181-4. Epub 2020 Mar 31.
Fibroblast growth factor 23 (FGF23) is a protein produced by mature osteoblasts involved in mineral homeostasis by binding to its receptor complex FGFR/Klotho located mainly in the kidneys. Although this protein participates in numerous biological processes, increase in the levels of FGF23 is responsible for many pathologies, such as X-linked hypophosphataemia (XLH), chronic kidney disease, cardiovascular disease or even mortality. For this reason, both FGF23 and its receptors have become elements of interest for the development of treatments. However, FGF23 can be altered for many other reasons, such as inflammatory processes, iron, hypoxia, heart failure or erythropoietin, that negatively affect mortality. This article will review the role of FGF23 in phosphate homeostasis, its relationship to mortality, fractures and chronic renal failure, and how the levels of this factor can be reduced.
成纤维细胞生长因子 23（FGF23）是一种由成熟成骨细胞产生的蛋白质，通过与主要位于肾脏中的受体复合物 FGFR/Klotho 结合，参与矿物质稳态的调节。尽管这种蛋白质参与了许多生物过程，但 FGF23 水平的增加与许多病理有关，如 X 连锁低磷血症（XLH）、慢性肾脏病、心血管疾病甚至死亡。因此，FGF23 及其受体已成为开发治疗方法的关注点。然而，FGF23 也可能因炎症过程、铁、缺氧、心力衰竭或促红细胞生成素等多种其他原因而发生改变，这些因素会对死亡率产生负面影响。本文将综述 FGF23 在磷酸盐稳态中的作用、它与死亡率、骨折和慢性肾衰竭的关系，以及如何降低这种因子的水平。
