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线粒体功能障碍对细胞功能的影响:在动脉粥样硬化中的作用。

Effects of mitochondrial dysfunction on cellular function: Role in atherosclerosis.

作者信息

Xu Minwen, Wang Wenjun, Cheng Jingpei, Qu Hongen, Xu Minjuan, Wang Liefeng

机构信息

Clinical Skills Center, First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, China.

Department of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.

出版信息

Biomed Pharmacother. 2024 May;174:116587. doi: 10.1016/j.biopha.2024.116587. Epub 2024 Apr 17.

DOI:10.1016/j.biopha.2024.116587
PMID:38636397
Abstract

Atherosclerosis, an immunoinflammatory disease of medium and large arteries, is associated with life-threatening clinical events, such as acute coronary syndromes and stroke. Chronic inflammation and impaired lipoprotein metabolism are considered to be among the leading causes of atherosclerosis, while numerous risk factors, including arterial hypertension, diabetes mellitus, obesity, and aging, can contribute to the development of the disease. In recent years, emerging evidence has underlined the key role of mitochondrial dysfunction in the pathogenesis of atherosclerosis. Mitochondrial dysfunction is believed to result in an increase in reactive oxygen species, leading to oxidative stress, chronic inflammation, and intracellular lipid deposition, all of which can contribute to the pathogenesis of atherosclerosis. Critical cells, including endothelial cells, vascular smooth muscle cells, and macrophages, play an important role in atherosclerosis. Mitochondrial function is also involved in maintaining the normal function of these cells. To better understand the relationship between mitochondrial dysfunction and atherosclerosis, this review summarizes the findings of recent studies and discusses the role of mitochondrial dysfunction in the risk factors and critical cells of atherosclerosis. FACTS: OPEN QUESTIONS.

摘要

动脉粥样硬化是一种发生于中、大动脉的免疫炎症性疾病,与急性冠脉综合征和中风等危及生命的临床事件相关。慢性炎症和脂蛋白代谢受损被认为是动脉粥样硬化的主要病因,而包括动脉高血压、糖尿病、肥胖和衰老在内的众多风险因素都可能促使该疾病的发展。近年来,新出现的证据强调了线粒体功能障碍在动脉粥样硬化发病机制中的关键作用。线粒体功能障碍被认为会导致活性氧增加,进而引发氧化应激、慢性炎症和细胞内脂质沉积,所有这些都可能促成动脉粥样硬化的发病机制。关键细胞,包括内皮细胞、血管平滑肌细胞和巨噬细胞,在动脉粥样硬化中起重要作用。线粒体功能也参与维持这些细胞的正常功能。为了更好地理解线粒体功能障碍与动脉粥样硬化之间的关系,本综述总结了近期研究的结果,并讨论了线粒体功能障碍在动脉粥样硬化的风险因素和关键细胞中的作用。事实:有待解决的问题。

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