HMGB1: A critical mediator for oxidized-low density lipoproteins induced atherosclerosis.
HMGB1: A critical mediator for oxidized-low density lipoproteins induced atherosclerosis.
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DOI：
10.1016/j.ijcard.2015.08.203
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发表时间：
2016
影响因子：
3.5
通讯作者：
Qin Zhou;Zhaowei Zhu;Xinqun Hu;C. Shu
中科院分区：
文献类型：
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作者：
Qin Zhou;Zhaowei Zhu;Xinqun Hu;C. Shu
我们最近饶有兴趣地阅读了 Mollace V 和学院的报告 [1]，内容涉及“氧化 LDL 减弱保护性自噬并诱导内皮细胞凋亡：氧化应激和 LOX-1 受体表达的作用”。他们表明，氧化低密度脂蛋白会导致内皮细胞中 NO 生成受损和细胞凋亡。这种效应是通过 LOX-1 的过度表达和随后保护性自噬反应的减弱而发生的，从而导致氧化低密度脂蛋白诱导的内皮功能障碍的病理生理学，这是动脉粥样硬化过程早期阶段的特征。
We have recently read with great interest the report by Mollace V and colleges [1] concerning" Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression." They indicate that oxidized-low density lipoproteins leads to impaired NO generation and apoptotic cell death in endothelial cells. This effect occurs via the overexpression of LOX-1 and subsequent attenuation of protective autophagic response thereby contributing to the pathophysiology of oxidized-low density lipoproteins-induced endothelial dysfunction which characterizes early stages of atherosclerotic process.