内皮细胞损伤在糖尿病肾病发病机制中的作用

被引:161
作者
赵鹏鸣
王俭勤
梁耀军
机构
[1] 兰州大学第二医院肾内科
关键词
肾小球内皮细胞; 糖尿病肾病; 蛋白尿; 发病机制;
D O I
暂无
中图分类号
R587.2 [糖尿病性昏迷及其他并发症]; R692.9 [其他疾病];
学科分类号
100201 [内科学]; 100221 [泌尿外科学];
摘要
DN是糖尿病慢性微血管并发症之一,也是引起终末期肾病和导致糖尿病患者死亡的主要原因。肾小球内皮细胞是肾小球滤过屏障的重要组分,因其与循环物质直接接触,易受血糖、血脂及炎症因子损伤的影响。高血糖状态下,蛋白激酶C(PKC)通路、多元醇通路和氧化应激(OS)被激活,并产生过量的AGEs和活性氧簇(ROS),损伤内皮一氧化氮合酶(eNOS),降低一氧化氮的生成,同时高血糖刺激RAS产生大量血管紧张素Ⅱ损伤内皮细胞,此外,肾小球足细胞与内皮细胞相互作用,进一步加重内皮细胞损伤。本文就内皮细胞损伤在DN发病机制中的作用做一综述。
引用
收藏
页码:169 / 172
页数:4
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