Fibroblast growth factor 23 (FGF23) was initially characterized as an important regulator of phosphate and calcium homeostasis. New research advances demonstrate that FGF23 is also linked to iron economy, inflammation and erythropoiesis. These advances have been fuelled, in part, by the serendipitous development of two distinct FGF23 assays that can substitute for invasive bone biopsies to infer the activity of the three main steps of FGF23 regulation in bone: transcription, post-translational modification and peptide cleavage. This ‘liquid bone biopsy for FGF23 dynamics’ enables large-scale longitudinal studies of FGF23 regulation that would otherwise be impossible in humans. The balance between FGF23 production, post-translational modification and cleavage is maintained or perturbed in different hereditary monogenic conditions and in acquired conditions that mimic these genetic disorders, including iron deficiency, inflammation, treatment with ferric carboxymaltose and chronic kidney disease. Looking ahead, a deeper understanding of the relationships between FGF23 regulation, iron homeostasis and erythropoiesis can be leveraged to devise novel therapeutic targets for treatment of anaemia and states of FGF23 excess, including chronic kidney disease.

成纤维细胞生长因子 23 (FGF23) 最初被描述为磷酸盐和钙稳态的重要调节剂。新的研究进展表明，FGF23 还与铁经济、炎症和红细胞生成有关。这些进展的部分原因是偶然开发了两种不同的 FGF23 检测方法，这些检测方法可以替代侵入性骨活检来推断骨中 FGF23 调节的三个主要步骤的活性：转录、翻译后修饰和肽切割。这种“用于 FGF23 动力学的液体骨活检”能够对 FGF23 调控进行大规模纵向研究，而这在人类中是不可能的。FGF23生产之间的平衡，在不同的遗传性单基因条件和模仿这些遗传疾病的获得性条件下，包括缺铁、炎症、用羧基麦芽糖铁治疗和慢性肾病，翻译后修饰和切割得以维持或受到干扰。展望未来，可以利用对 FGF23 调节、铁稳态和红细胞生成之间关系的更深入了解来设计治疗贫血和 FGF23 过量状态（包括慢性肾病）的新治疗靶点。