FGF23 病理生理学的非肾脏相关机制。
Non-renal-Related Mechanisms of FGF23 Pathophysiology.
机构信息
UCLA Department of Pediatrics, Division of Pediatric Nephrology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC A2-383, Los Angeles, CA, 90095-1752, USA.
出版信息
Curr Osteoporos Rep. 2018 Dec;16(6):724-729. doi: 10.1007/s11914-018-0492-2.
PURPOSE OF REVIEW
We will review non-renal-related mechanisms of fibroblast growth factor 23 (FGF23) pathophysiology.
RECENT FINDINGS
FGF23 production and metabolism may be affected by many bone, mineral, and kidney factors. However, it has recently been demonstrated that other factors, such as iron status, erythropoietin, and inflammation, also affect FGF23 production and metabolism. As these non-mineral factors are especially relevant in the setting of chronic kidney disease (CKD), they may represent emerging determinants of CKD-associated elevated FGF23 levels. Moreover, FGF23 itself may promote anemia and inflammation, thus contributing to the multifactorial etiologies of these CKD-associated comorbidities. CKD-relevant, non-mineral-related, bidirectional relationships exist between FGF23 and anemia, and between FGF23 and inflammation. Iron deficiency, anemia, and inflammation affect FGF23 production and metabolism, and FGF23 itself may contribute to anemia and inflammation, highlighting complex interactions that may affect aspects of CKD pathogenesis and treatment.
综述目的
我们将回顾成纤维细胞生长因子 23（FGF23）病理生理学的非肾脏相关机制。
最近的发现
FGF23 的产生和代谢可能受到许多骨骼、矿物质和肾脏因素的影响。然而，最近已经证明，其他因素，如铁状态、促红细胞生成素和炎症，也会影响 FGF23 的产生和代谢。由于这些非矿物质因素在慢性肾脏病（CKD）的情况下尤其相关，因此它们可能代表与 CKD 相关的升高的 FGF23 水平的新兴决定因素。此外，FGF23 本身可能会导致贫血和炎症，从而导致这些 CKD 相关合并症的多因素病因。CKD 相关的、非矿物质相关的、双向的 FGF23 与贫血之间以及 FGF23 与炎症之间存在关系。铁缺乏、贫血和炎症会影响 FGF23 的产生和代谢，而 FGF23 本身可能会导致贫血和炎症，突出了可能影响 CKD 发病机制和治疗的复杂相互作用。
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