[1]王艺凯,郭利伟.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[J].新乡医学院学报,2023,40(11):1083-1086.[doi:10.7683/xxyxyxb.2023.11.015]
　WANG Yikai,GUO Liwei.Research progress on the mechanism of fibroblast growth factor 23-Klotho axis in vascular calcification[J].Journal of Xinxiang Medical University,2023,40(11):1083-1086.[doi:10.7683/xxyxyxb.2023.11.015]
点击复制

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
分享到：

《新乡医学院学报》[ISSN:1004-7239/CN:41-1186/R]

卷:
40卷
期数:
2023年11
页码:
1083-1086
栏目:
综述
出版日期:
2023-11-05

文章信息/Info

Title:
Research progress on the mechanism of fibroblast growth factor 23-Klotho axis in vascular calcification
作者:
王艺凯; 郭利伟
（新乡医学院法医学院，河南　新乡　453003）
Author(s):
WANG Yikai; GUO Liwei
(Department of Forensic Medicine，Xinxiang Medical University，Xinxiang 453003,Henan Province,China）
关键词:
血管钙化; 钙磷代谢; 成纤维细胞因子23; Klotho
Keywords:
vascular calcification; calcium and phosphorus metabolism; fibroblast growth factor 23; Klotho
分类号:
R544
DOI:
10.7683/xxyxyxb.2023.11.015
文献标志码:
A
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。
Abstract:
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.

参考文献/References:

［1］　BARALIC M,BRKOVIC V,STOJANOV V,et al.Dual roles of the mineral metabolism disorders biomarkers in prevalent hemodilysis patients:in renal bone disease and in vascular calcification［J］.J Med Biochem,2019,38(2):134-144.
［2］　CIANCIOLO G,GALASSI A,CAPELLI I,et al.Klotho-FGF23,cardiovascular disease,and vascular calcification:black or white［J］.Curr Vasc Pharmacol,2018,16(2):143-156.
［3］　DUSING P,ZIETZER A,GOODY P R,et al.Vascular pathologies in chronic kidney disease:pathophysiological mechanisms and novel therapeutic approaches［J］.J Mol Med (Berl),2021,99(3):335-348.
［4］　KURO O M.Phosphate as a pathogen of arteriosclerosis and aging［J］.J Atheroscler Thromb,2021,28(3):203-213.
［5］　KIM H J,KIM Y,KANG M,et al.Low Klotho/fibroblast growth factor 23 ratio is an independent risk factor for renal progression in chronic kidney disease:finding from KNOW-CKD［J］.Front Med (Lausanne),2022,9:904963.
［6］　HUM J M,O′BRYAN L,SMITH R C,et al.Novel functions of circulating Klotho［J］.Bone,2017,100:36-40.
［7］　GALASSI A,CUPISTI A,SANTORO A,et al.Phosphate balance in ESRD:diet,dialysis and binders against the low evident masked pool［J］.J Nephrol,2015,28(4):415-429.
［8］　COURBEBAISSE M,LANSKE B.Biology of fibroblast growth factor 23:from physiology to pathology［J］.Cold Spring Harb Perspect Med,2018,8(5):a031260.
［9］　FUJII H,YONEKURA Y,NAKAI K,et al.Comparison of the effects of novel vitamin D receptor analog VS-105 and paricalcitol on chronic kidney disease-mineral bone disorder in an experimental model of chronic kidney disease［J］.J Steroid Biochem Mol Biol,2017,167:55-60.
［10］　LIU E S,MARTINS J S,RAIMANN A,et al.1,25-dihydroxyvitamin D alone improves skeletal growth,microarchitecture,and strength in a murine model of XLH,despite enhanced FGF23 expression［J］.J Bone Miner Res,2016,31(5):929-939.
［11］　CARRILLO-LOPEZ N,MARTINEZ-ARIAS L,FERNANDEZ-VILLABRILLE S,et al.Role of the RANK/RANKL/OPG and wnt/beta-catenin systems in CKD bone and cardiovascular disorders［J］.Calcif Tissue Int,2021,108(4):439-451.
［12］　MACE M L,OLGAARD K,LEWIN E.New aspects of the kidney in the regulation of fibroblast growth factor 23 (FGF23) and mineral homeostasis［J］.Int J Mol Sci,2020,21(22):8810.
［13］　ERBEN R G,ANDRUKHOVA O.FGF23-Klotho signaling axis in the kidney［J］.Bone,2017,100:62-68.
［14］　TORBUS-PALUSZCZAK M,BARTMAN W,ADAMCZYK-SOWA M.Klotho protein in neurodegenerative disorders［J］.Neurol Sci,2018,39(10):1677-1682.
［15］　BUCHANAN S,COMBET E,STENVINKEL P,et al.Klotho,aging,and the failing kidney［J］.Front Endocrinol (Lausanne),2020,11:560.
［16］　HUM J M,O′BRYAN L M,TATIPARTHI A K,et al.Chronic hyperphosphatemia and vascular calcification are reduced by stable delivery of soluble Klotho［J］.J Am Soc Nephrol,2017,28(4):1162-1174.
［17］　LI L,LIU W,MAO Q,et al.Klotho ameliorates vascular calcification via promoting autophagy［J］.Oxid Med Cell Longev,2022,2022:7192507.
［18］　PRUD′HOMME G J,KURT M,WANG Q.Pathobiology of the Klotho antiaging protein and therapeutic considerations［J］.Front Aging,2022,3:931331.
［19］　CHEN Y,MAO C,GU R,et al.Nidogen-2 is a novel endogenous ligand of LGR4 to inhibit vascular calcification［J］.Circ Res,2022,131(12):1037-1054.
［20］　EVRARD S,DELANAYE P,KAMEL S,et al.Vascular calcification:from pathophysiology to biomarkers［J］.Clin Chim Acta,2015,438:401-414.
［21］　ZUNUNI VAHED S,MOSTAFAVI S,HOSSEINIYAN KHATIBI S M,et al.Vascular calcification:an important understanding in nephrology［J］.Vasc Health Risk Manag,2020,16:167-180.
［22］　SHALHOUB V,SHATZEN E M,WARD S C,et al.FGF23 neutralization improves chronic kidney disease-associated hyperparathyroidism yet increases mortality［J］.J Clin Invest,2012,122(7):2543-2553.
［23］　SHIMADA T,URAKAWA I,YAMAZAKI Y,et al.FGF-23 transgenic mice demonstrate hypophosphatemic rickets with reduced expression of sodium phosphate cotransporter type IIa［J］.Biochem Biophys Res Commun,2004,314(2):409-414.
［24］　MUNOZ-CASTANEDA J R,RODELO-HAAD C,PENDON-RUIZ DE MIER M V,et al.Klotho/FGF23 and wnt signaling as important players in the comorbidities associated with chronic kidney disease［J］.Toxins (Basel),2020,12(3):185.
［25］　CHEN Y X,HUANG C,DUAN Z B,et al.Klotho/FGF23 axis mediates high phosphate-induced vascular calcification in vascular smooth muscle cells via Wnt7b/beta-catenin pathway［J］.Kaohsiung J Med Sci,2019,35(7):393-400.
［26］　CARRILLO-LOPEZ N,PANIZO S,ALONSO-MONTES C,et al.Direct inhibition of osteoblastic Wnt pathway by fibroblast growth factor 23 contributes to bone loss in chronic kidney disease［J］.Kidney Int,2016,90(1):77-89.
［27］　ZHENG S,ZHANG S,SONG Y,et al.MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23［J］.Iran J Basic Med Sci,2016,19(12):1331-1336.
［28］　KUCZERA P,ADAMCZAK M,WIECEK A.Fibroblast growth factor-23:a potential uremic toxin［J］.Toxins (Basel),2016,8(12):369.
［29］　KURO O M.Aging and FGF23-klotho system［J］.Vitam Horm,2021,115:317-332.
［30］　SALANOVA VILLANUEVA L,SANCHEZ GONZALEZ C,SANCHEZ TOMERO J A,et al.Bone mineral disorder in chronic kidney disease:Klotho and FGF23;cardiovascular implications［J］.Nefrologia,2016,36(4):368-375.
［31］　BOYCE B F,XING L.Functions of RANKL/RANK/OPG in bone modeling and remodeling［J］.Arch Biochem Biophys,2008,473(2):139-146.
［32］　YASUDA H.Discovery of the RANKL/RANK/OPG system［J］.J Bone Miner Metab,2021,39(1):2-11.
［33］　ALLARD L,DEMONCHEAUX N,MACHUCA-GAYET I,et al.Biphasic effects of vitamin D and FGF23 on human osteoclast biology［J］.Calcif Tissue Int,2015,97(1):69-79.
［34］　NAKAHARA T,KAWAI-KOWASE K,MATSUI H,et al.Fibroblast growth factor 23 inhibits osteoblastic gene expression and induces osteoproteger in vascular smooth muscle cells［J］.Atherosclerosis,2016,253:102-110.
［35］　FITZPATRICK J,KIM E D,SOZIO S M,et al.Calcification biomarkers,subclinical vascular disease,and mortality among multie-thnic dialysis patients［J］.Kidney Int Rep,2020,5(10):1729-1737.
［36］　HU M C,SHI M,ZHANG J,et al.Klotho deficiency causes vascular calcification in chronic kidney disease［J］.J Am Soc Nephrol,2011,22(1):124-136.
［37］　ZHAO Y,ZHAO M M,CAI Y,et al.Mammalian target of rapamycin signaling inhibition ameliorates vascular calcification via Klotho upregulation［J］.Kidney Int,2015,88(4):711-721.
［38］　MUNOZ-CASTANEDA J R,HERENCIA C,PENDON-RUIZ DE MIER M V,et al.Differential regulation of renal Klotho and FGFR1 in normal and uremic rats［J］.FASEB J,2017,31(9):3858-3867.
［39］　CHEN T,MAO H,CHEN C,et al.The role and mechanism of alpha-Klotho in the calcification of rat aortic vascular smooth muscle cells［J］.Biomed Res Int,2015,2015:194362.

相似文献/References:

[1]夏　雪,肖　蓓,林　辉.终末期肾脏病患者血管钙化和血清骨硬化蛋白水平分析[J].新乡医学院学报,2020,37(8):758.[doi:10.7683/xxyxyxb.2020.08.013]
　XIA Xue,XIAO Bei,LIN Hui.Analysis of vascular calcification and serum sclerostin level in patients with end-stage renal disease[J].Journal of Xinxiang Medical University,2020,37(11):758.[doi:10.7683/xxyxyxb.2020.08.013]
[2]石新慧,任东升,陶雅非,等.血清sclerostin和Klotho蛋白水平对维持性血液透析患者血管钙化的预测价值[J].新乡医学院学报,2022,39(5):429.[doi:10.7683/xxyxyxb.2022.05.006]
　SHI Xinhui,REN Dongsheng,TAO Yafei,et al.Predictive value of serum sclerostin and Klotho protein levels for angiosteosis in patients undergoing maintenance hemodialysis[J].Journal of Xinxiang Medical University,2022,39(11):429.[doi:10.7683/xxyxyxb.2022.05.006]
[3]鲁　冰,任东升,陶雅非,等.维持性血液透析与持续不卧床腹膜透析对终末期肾病患者钙磷代谢及氧化应激的影响比较[J].新乡医学院学报,2022,39(9):833.[doi:10.7683/xxyxyxb.2022.09.007]
　LU Bing,REN Dongsheng,TAO Yafei,et al.Comparison of the effect of maintenance hemodialysis and continuous ambulatory peritoneal dialysis on calcium and phosphorus metabolism and oxidative stress in patients with end-stage renal disease[J].Journal of Xinxiang Medical University,2022,39(11):833.[doi:10.7683/xxyxyxb.2022.09.007]

更新日期/Last Update: 2023-11-05