成纤维细胞因子23-Klotho轴在血管钙化中的作用机制研究进展  

Research progress on the mechanism of fibroblast growth factor 23-Klotho axis in vascular calcification

作　　者：王艺凯 郭利伟 WANG Yikai;GUO Liwei(Department of Forensic Medicine,Xinxiang Medical University,Xinxiang 453003,Henan Province,China)

机构地区：[1]新乡医学院法医学院,河南新乡453003

出　　处：《新乡医学院学报》2023年第11期1083-1086,共4页Journal of Xinxiang Medical University

基　　金：国家自然科学基金资助项目(编号:81900391);河南省科技攻关计划项目(编号:182102310240)。

摘　　要：血管钙化(VC)与心血管疾病和慢性肾脏病患者全因死亡风险高度相关。VC的发病机制复杂,钙磷代谢失调是导致VC的主要原因。成纤维细胞因子23(FGF23)是由骨细胞和骨原细胞合成的具有内分泌功能的蛋白质,通过共受体Klotho作用于肾脏和甲状旁腺而调节钙磷代谢。近年来,关于FGF23及其共受体Klotho的研究在解释VC方面取得了显著进展,本文就FGF23和Klotho在VC中的作用和机制进行综述,旨在为VC相关心血管疾病及肾脏疾病的预防和治疗提供理论基础和新靶点。Vascular calcification(VC)is highly associated with the risk of all-cause death in patients with cardiovascular disease and chronic kidney disease.Pathogenesis of VC is complex,and the imbalance of calcium and phosphorus metabolism is the main cause of VC.Fibroblast growth factor 23(FGF23)is a protein secreted by bone cells and osteoblasts,which acts on the kidney and parathyroid gland through the Klotho receptor to regulate calcium and phosphorus metabolism.Recent data on FGF23 and Klotho have made remarkable progress in the interpretation of VC.This paper reviews the role and mechanism of FGF23 and Klotho in VC,aiming to provide new targets for the prevention and treatment of VC-related cardiovascular and renal diseases.

关 键 词：血管钙化 钙磷代谢 成纤维细胞因子23 KLOTHO 

分 类 号：R544[医药卫生—心血管疾病]