Atherosclerosis: From the Disruption of Mitochondrial Membrane Potential to the Potential Interventional Strategies

被引:4
|
作者
Xia, Dexiang [1 ]
Chen, Yanmei [1 ]
Luo, Guifang [2 ]
Wei, Dangheng [1 ]
机构
[1] Univ South China, Inst Cardiovasc Dis, Hengyang Med Sch,Key Lab Arteriosclerol Hunan, Hunan Int Sci & Technol Corp Base Arteriosc, Hengyang 421001, Hunan, Peoples R China
[2] Univ South China, Dept Gynecol, Affiliated Hosp 1, Hengyang 421001, Peoples R China
基金
中国国家自然科学基金;
关键词
Atherosclerosis (AS); mitochondrial membrane potential (deltapsi (m)); therapeutics; reactive oxygen species (ROS); apoptosis; NLRP3; inflammasome; NLRP3 INFLAMMASOME ACTIVATION; SMOOTH-MUSCLE-CELL; BETA-CAROTENE; VITAMIN-E; MACROPHAGE APOPTOSIS; OXIDATIVE STRESS; CARDIOVASCULAR-DISEASE; SUPEROXIDE-DISMUTASE; IN-VIVO; ATTENUATES ATHEROSCLEROSIS;
D O I
10.2174/0929867330666221201120405
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Atherosclerosis (AS) is the major factor of cardiovascular disease (CVD) and is characterized by a progressive and chronic inflammatory process in the arterial wall. Recent studies have shown that disruption of the mitochondrial membrane potential (deltapsi (m)) directly affects the electron transport chain (ETC), which in turn leads to oxidative stress, and furthermore, its alteration leads to apoptosis and activation of the NLRP3 inflammasome, thereby promoting the development of AS. Here, this review describes how deltapsi (m) contributes to the development of AS by mediating oxidative stress, apoptosis, and NLRP3 inflammasome activation, and potential AS intervention strategies by targeting oxidative stress, apoptosis, and NLRP3 inflammasome activation induced by deltapsi (m).
引用
收藏
页码:4355 / 4373
页数:19
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