氧化应激在糖尿病性心血管疾病中的研究进展附视频

被引：14

作者：

练淑平 ^{[1
]}

张耀 ^{[2
]}

王振花 ^{[3
]}

机构：

[1] 广东医科大学研究生学院

[2] 深圳市宝安区中心医院心血管内科

[3] 深圳市宝安区人民医院心血管内科

来源：

医学综述 | 2019年 / 10期

关键词：

糖尿病; 心血管疾病; 氧化应激;

D O I：

暂无

中图分类号：

R587.2 [糖尿病性昏迷及其他并发症]; R54 [心脏、血管（循环系）疾病];

学科分类号：

摘要：

糖尿病性心血管疾病是糖尿病患者的慢性并发症之一,其发病机制包括氧化应激的产生、晚期糖基化终末产物和蛋白激酶C（PKC）的激活等。其中,活性氧类的生成增加被认为是导致糖尿病性心血管疾病的核心机制。氧化应激可通过直接或间接激活核因子κB、p38促分裂原活化的蛋白激酶、PKC、肾素-血管紧张素-醛固酮系统等路径,引起炎症、内皮细胞功能障碍、动脉粥样硬化、心肌细胞肥大、凋亡和心肌纤维化,导致严重的心脏功能障碍。未来,深入了解氧化应激在糖尿病性心血管疾病的病理生理机制将为其预防和治疗提供理论依据。

引用

页码：2029 / 2033

页数：5

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