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LOX-1, oxidant stress, mtDNA damage, autophagy, and immune response in atherosclerosis

机译:LOX-1,动脉粥样硬化中的氧化应激,mtDNA损伤,自噬和免疫反应

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摘要

As a major receptor for oxidized low density lipoprotein (ox-LDL), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is upregulated in many pathophysiological events, including endothelial cell dysfunction and smooth muscle cell growth, as well as monocyte migration and transformation into foam cells, which are present in atherosclerosis and myocardial ischemia. Excessive production of reactive oxygen species (ROS) increases LOX-1 expression, induces mitochondrial DNA damage, and activates autophagy. Damaged mitochondrial DNA that escapes from autophagy induces an inflammatory response. This paper reviews the potential link between LOX-1, mitochondrial DNA damage, autophagy, and immune response in atherosclerosis.
机译:作为氧化型低密度脂蛋白(ox-LDL)的主要受体,凝集素样氧化型低密度脂蛋白受体1(LOX-1)在许多病理生理事件中均被上调,包括内皮细胞功能障碍和平滑肌细胞生长单核细胞迁移并转化为泡沫细胞,而泡沫细胞存在于动脉粥样硬化和心肌缺血中。过量产生活性氧(ROS)会增加LOX-1的表达,诱导线粒体DNA损伤并激活自噬。逃脱自噬的线粒体DNA受损会引起炎症反应。本文综述了动脉粥样硬化中LOX-1,线粒体DNA损伤,自噬和免疫反应之间的潜在联系。

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