Importance of NLRP3 Inflammasome in Abdominal Aortic Aneurysms

被引:30
作者
Shi, Jinyun [1 ]
Guo, Jia [1 ]
Li, Zhidong [2 ]
Xu, Baohui [3 ]
Miyata, Masaaki [4 ]
机构
[1] Shanxi Med Univ, Ctr Hypertens Care, Hosp 1, Taiyuan, Shanxi, Peoples R China
[2] Shanxi Med Univ, Dept Pharmacol, Taiyuan, Shanxi, Peoples R China
[3] Stanford Univ, Dept Surg, Sch Med, Stanford, CA USA
[4] Kagoshima Univ, Fac Med, Sch Hlth Sci, Kagoshima, Japan
基金
中国国家自然科学基金;
关键词
Abdominal aortic aneurysm; Inflammasome; NLRP3; Interleukin-1; Interleukin-18; OXIDATIVE STRESS; DIPEPTIDYL PEPTIDASE-4; GENE-EXPRESSION; INHIBITOR; INTERLEUKIN-1-BETA; GROWTH; PROGRESSION; ACTIVATION; ATHEROSCLEROSIS; DIFFERENTIATION;
D O I
10.5551/jat.RV17048
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Abdominal aortic aneurysm (AAA) is a chronic inflammatory degenerative aortic disease, which particularly affects older people. Nucleotide-binding oligomerization domain-like receptor family protein 3 (NLRP3) inflammasome is a multi-protein complex and mediates inflammatory responses by activating caspase 1 for processing premature interleukin (IL)-1 beta and IL-18. In this review, we first summarize the principle of NLRP3 inflammasome activation and the functionally distinct classes of small molecule NLRP3 inflammasome inhibitors. Next, we provide a comprehensive literature review on the expression of NLRP3 inflammasome effector mediators (IL-1 beta and IL-18) and components (caspase 1, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and NLRP3) in clinical and experimental AAAs. Finally, we discuss the influence of genetic deficiency or pharmacological inhibition of individual effector mediators and components of NLRP3 inflammasome on experimental AAAs. Accumulating clinical and experimental evidence suggests that NLRP3 inflammasome may be a promise therapeutic target for developing pharmacological strategies for clinical AAA management.
引用
收藏
页码:454 / 466
页数:13
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