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成纤维细胞生长因子 23 在急性肾损伤中的研究进展。

Research progress of fibroblast growth factor 23 in acute kidney injury.

机构信息

Division of Nephrology, Department of Medicine, West China Hospital, Sichuan University, 37 Guoxue Lane, Chengdu, 610041, Sichuan, China.

Division of Nephrology, Henan Key Laboratory for Kidney Disease and Immunology, Henan Provincial People's Hospital, Zhengzhou, Henan, China.

出版信息

Pediatr Nephrol. 2023 Jul;38(7):2013-2022. doi: 10.1007/s00467-022-05791-z. Epub 2022 Nov 22.

Abstract

Fibroblast growth factor 23 (FGF23) is primarily produced in bones and mainly regulates calcium and phosphorus metabolism. The level of circulating FGF23 increases rapidly in the early stage of acute kidney injury (AKI). Recent studies have shown that FGF23 may serve as a biomarker for the diagnosis and poor prognosis of AKI. The mechanism of increased FGF23 in AKI may include increased production of FGF23, decreased renal clearance of FGF23, and some new regulatory factors, such as inflammation and glycerol 3-phosphate. However, the biological effects of elevated FGF23 in AKI are still unclear. It is also not known whether reducing the level of circulating FGF23 could alleviate AKI or its poor prognosis. Here, we review the pathophysiological mechanism and possible regulation of FGF23 in AKI and discuss the possibility of using FGF23 as a therapeutic target.

摘要

成纤维细胞生长因子 23(FGF23)主要在骨骼中产生,主要调节钙和磷代谢。在急性肾损伤(AKI)的早期,循环 FGF23 的水平迅速升高。最近的研究表明,FGF23 可能作为 AKI 的诊断和预后不良的生物标志物。AKI 中 FGF23 增加的机制可能包括 FGF23 产生增加、FGF23 的肾脏清除减少以及一些新的调节因子,如炎症和甘油磷酸。然而,AKI 中升高的 FGF23 的生物学效应尚不清楚。也不知道降低循环 FGF23 的水平是否可以减轻 AKI 或其预后不良。在这里,我们综述了 FGF23 在 AKI 中的病理生理机制和可能的调节作用,并讨论了将 FGF23 作为治疗靶点的可能性。

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