慢性肾脏病血管钙化发病机制的研究进展  

Research progress on pathogenesis of vascular calcification in chronic kidney disease

作　　者：徐莹[1] 李鑫(综述)[1] 郝丽荣(审校)[1] XU Ying;LI Xin;HAO Lirong(Department of Nephropathy,First Affiliated Hospital,Harbin Medical University,Harbin 150001,China)

机构地区：[1]哈尔滨医科大学附属第一医院肾内科,哈尔滨150001

出　　处：《临床与病理杂志》2021年第6期1399-1404,共6页Journal of Clinical and Pathological Research

基　　金：国家自然科学基金(81870503)。

摘　　要：血管钙化(vascular calcification,VC)是慢性肾脏病(chronic kidney disease,CKD)患者心血管病死率高的主要原因。VC发病机制非常复杂,与肾的排泄功能、内分泌功能减退等相关,如明显的钙磷代谢紊乱、klotho蛋白水平降低、炎症氧化应激和细胞凋亡、钙化抑制因子的减少和尿毒症毒素的累积等。近年来发现的micro RNA的调控也与VC密切相关,其中多种过程介导的VC涉及血管平滑肌细胞的转分化。Vascular calcification(VC)is the main cause of high cardiovascular mortality in patients with chronic kidney disease(CKD).The pathogenesis is very complicated,and it is related to the decline of excretory function and endocrine function of the kidney,such as obvious calcium and phosphorus metabolism disorders,decrease of klotho protein,inflammatory oxidative stress and apoptosis,reduction of calcification inhibitory factors,and accumulation of uremic toxins.In addition,the regulation of micro RNA discovered in recent years is also closely related to VC,among which VC mediated by multiple processes is involved in the transdifferentiation of vascular smooth muscle cells.

关 键 词：血管钙化 慢性肾脏病 高磷血症 血管平滑肌细胞 

分 类 号：R692[医药卫生—泌尿科学]