慢性肾脏病血管钙化机制的研究进展

doi:10.16352/j.issn.1001-6325.2022.07.1124

基础医学与临床 ›› 2022, Vol. 42 ›› Issue (7): 1124-1128.doi: 10.16352/j.issn.1001-6325.2022.07.1124

慢性肾脏病血管钙化机制的研究进展

熊浩, 袁芳^*

中南大学湘雅二医院肾内科, 湖南长沙 410011

收稿日期:2021-03-08 修回日期:2021-07-17 出版日期:2022-07-05 发布日期:2022-06-29
通讯作者: * 1278018214@qq.com
基金资助:
国家自然科学基金(81770730)

Research progress on vascular calcification mechanism for chronic kidney disease

XIONG Hao, YUAN Fang^*

Department of Nephrology,the Second Xiangya Hospital,Central South University,Changsha 410011,China

Received:2021-03-08 Revised:2021-07-17 Online:2022-07-05 Published:2022-06-29
Contact: * 1278018214@qq.com

摘要/Abstract

摘要： 心血管事件是慢性肾脏病(CKD)及终末期肾病(ESRD)患者主要的死亡原因。研究认为血管钙化是导致心血管事件的独立危险因素。应除了传统心血管事件的预防,在CKD患者中,关注血管钙化发生机制、平衡促钙化因素与抑钙化因素,是慢性肾脏病矿物质-骨代谢异常(CKD-MBD)防治首要关注的问题。

关键词: 慢性肾脏病, 血管钙化, 钙磷代谢, FGF23/Klotho, 炎性损伤

Abstract: Cardiovascular events are the main cause of death in chronic kidney disease(CKD) and end stage renal disease(ESRD).Studies have shown that vascular calcification is an independent risk factor for cardiovascular events.In addition to the prevention of cardiovascular events,paying attention to the mechanism of vascular calcification, keeping balance of pro-calcification factors and anti-calcification factors should be the primary concerns in prevention and treatment of chronic kidney disease with CKD-mineral and bone disorder(CKD-MBD) in CKD patients.

Key words: chronic kidney disease, vascular calcification, calcium and phosphate metabolism, FGF23/Klotho, inflammatory injury

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熊浩, 袁芳. 慢性肾脏病血管钙化机制的研究进展[J]. 基础医学与临床, 2022, 42(7): 1124-1128.

XIONG Hao, YUAN Fang. Research progress on vascular calcification mechanism for chronic kidney disease[J]. Basic & Clinical Medicine, 2022, 42(7): 1124-1128.

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参考文献 22

[1]	Jorge B,Beatriz M,Julia M,et al.Chronic kidney disease-mineral and bone disorders: pathogenesis and management[J].Calcif Tissue Int,2020,15.doi:10.1007/s00223-020-00777-1.
[2]	Michael P,Paul D.Current understanding of mineral and bone disorders of chronic kidney disease and the scientific grounds on the use of exogenous parathyroid hormone in its management[J].JBM J Bone Metab,2020,27:1-13.
[3]	Kim HJ,Kang E,Kim Y,et al.The association between soluble klotho and cardiovascular parameters in chronic kidney disease:results from the KNOW-CKD study[J].BMC Nephrol,2018,19:51-59.
[4]	Zhang M, Yan J, Zhu M, et al.Fibroblast growth factor 23 predicts coronary calcification and poor prognosis in patients with chronic kidney disease stages 3-5D[J]. Ann Clin Lab Sci,2015,45: 17-22.
[5]	Albanese I, Khan K, Barratt B, et al. Atherosclerotic calcification: Wnt is the Hint[J]. J Am Heart Assoc,2018,7:e007356.doi:10.1161/JAHA.117.007356.
[6]	Nakahara T, Dweck MR, Narula N, et al. Coronary artery calcification: from mechanism to molecular imaging[J]. JACC Cardiovasc Imaging,2017,10:582-593.
[7]	Voelkl J,Cejka D,Alesutan I.An overview of the mechanisms in vascular calcification during chronic kidney disease[J].Curr Opin Nephrol Hypertens, 2019, 28:289-296.
[8]	Matsumoto T, Takayanagi K, Kojima M, et al.Acute exposure to indoxyl sulfate impairs endotheliumdependent vasorelaxation in rat aorta[J]. Int J Mol Sci,2019,20:338-352.
[9]	Tang WH, Wang CP, Yu TH, et al. Protein-bounded uremic toxin p-cresylsulfate induces vascular permeability alternations[J]. Histochem Cell Biol,2018,149:607-617.
[10]	Rodriguez M,Rodriguez M.Recent advances in understanding and managing secondary hyperparathyroidism in chronic kidney disease[J].F1000Res,2020,9:dio:10.12688/f1000research.22636.1.
[11]	Hernandes FR, Canziani M, Barreto FC, et al. The shift from high to low turnover bone disease after parathyroidectomy is associated with the progression of vascular calcification in hemodialysis patients: a 12-month follow-up study[J]. PLoS One,2017,12:e0174811.doi:10.137/journal.pone.0174811.
[12]	Roumeliotis S,Dounousi E,Salmas M,et al.Vascular calcification in chronic kidney disease: the role of vitamin K-dependent matrix Gla protein[J].Front Med,2020,7:154-161.
[13]	Ruderman I, Holt SG, Hewitson TD, et al. Current and potential therapeutic strategies for the management of vascular calcification in patients with chronic kidney disease including those on dialysis[J]. Semin Dial,2018,31:487-499.
[14]	Shishkova D,Velikanova E, Sinitsky M, et al.Calcium phosphate bions cause intimal hyperplasia in intact aortas of normolipidemic rats through endothelial injury[J]. Int J Mol Sci. 2019, 20, 5728.doi:10.3390/ijms20225728.
[15]	Bielesz B, Reiter T, Marculescu R, et al. Calcification propensity of serum is independent of excretory renal function[J]. Sci Rep,2017,7:17941.doi:10.1038/s41598-017-18336-4.
[16]	Sheng K, Zhang P, Lin W, et al. Association of matrix Gla protein gene (rs1800801, rs1800802, rs4236) polymorphism with vascular calcifification and atherosclerotic disease: a meta-analysis[J]. Sci Rep,2017,7:8713.doi:10.1038/s41598-017-09328-5.
[17]	Li JS, Li B.Renal injury repair: how about the role of stem cells[J]. Adv Exp Med Biol,2019,1165:661-670.
[18]	Vervoet M,Cozzolino M.Vascular calcification in end-stage renal disease[J].Hemodial Int,2013,17:S17-S21.
[19]	Palmer SC,Mavridis D,Johnson DW,et al.Comparative effectiveness of calcimetic agents for secondary hyperparathyroidism in adults:a systematic review and network meta-analysis[J].Am J Kidney Dis,2020,76:321-330.
[20]	商瑀家,李玉霞,宋佳新,等.钙敏感受体在动脉粥样硬化中的作用研究进展[J].基础医学与临床,2020,40:395-398.
[21]	Parfrey PS,Drueke TB,Block GA,et al.The effects of cinacalcet in older and younger patients on hemodialysis:the evaluation of cinacalcet HCI therapy to lower cardiova-scular events(EVOLVE) trial[J].Clin J Am Soc Nephrol,2015,10:791-199.
[22]	刘志红,李贵森.中国慢性肾脏病矿物质和骨异常诊治指南[M].北京: 人民卫生出版社,2018:49-72.

慢性肾脏病血管钙化机制的研究进展

Research progress on vascular calcification mechanism for chronic kidney disease

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