Department of Genetics, Cytology and Bioengineering, Faculty of Biology and Medicine, Voronezh State University, Voronezh, Russia.
Laboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, 121552 Moscow, Russia.
Front Biosci (Elite Ed). 2020 Jan 1;12(1):102-112. doi: 10.2741/E860.
Atherosclerosis is a complex disorder that involves several mechanisms of pathogenesis tightly related to each other: lipid accumulation, inflammation and structural changes in the arterial wall. The main source of lipids accumulating in the arterial wall is low-density lipoprotein (LDL) atherogenically modified by desialylation or oxidation. Oxidized LDL can be produced as a result of enhanced generation of reactive oxygen species by mitochondria during oxidative stress. Mitochondrial dysfunction was found to be involved in every aspect of atherosclerosis, and is currently evaluated as a potential point of therapeutic intervention. In particular, atherosclerosis-associated inflammation and its link to mitochondrial dysfunction appear to be interesting, since mitochondria not only trigger the response to external signals, but also can act as pro-inflammatory agents themselves. In this regard, atherosclerosis is potentially an autoimmune disease. In this review, we summarize recent insights on the role of mitochondrial dysfunction in atherogenesis and discuss the significance of mitochondria for understanding of molecular basis of cardiovascular diseases.
动脉粥样硬化是一种复杂的疾病，涉及到几个紧密相关的发病机制：脂质积累、炎症和动脉壁的结构变化。在动脉壁中积累的脂质的主要来源是经过唾液酸或氧化修饰的低密度脂蛋白（LDL）。氧化的 LDL 可以通过氧化应激期间线粒体中活性氧的增强生成而产生。线粒体功能障碍被发现涉及动脉粥样硬化的各个方面，并且目前被评估为潜在的治疗干预点。特别是，与动脉粥样硬化相关的炎症及其与线粒体功能障碍的联系似乎很有趣，因为线粒体不仅触发对外界信号的反应，而且本身也可以作为促炎剂。在这方面，动脉粥样硬化可能是一种自身免疫性疾病。在这篇综述中，我们总结了线粒体功能障碍在动脉粥样形成中的作用的最新见解，并讨论了线粒体对于理解心血管疾病分子基础的重要性。
