NLRP3 inflammasome in sepsis

被引:28
作者
Shi, Xueyan [1 ]
Tan, Sichuang [2 ]
Tan, Sipin [1 ]
机构
[1] Cent South Univ, Dept Sepsis Translat Med, Key Lab Hunan Prov, Xiangya Sch Med, 88 Xiangya Rd, Changsha 410008, Hunan, Peoples R China
[2] Cent South Univ, Xiangya Hosp 2, Dept Thorac Surg, 139 Renmin Rd, Changsha 410008, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
NLRP3; inflammasome; activation; ubiquitination; phosphorylation; sepsis; NF-KAPPA-B; ACUTE KIDNEY INJURY; CASPASE-1; ACTIVATION; CATHEPSIN-B; INTERLEUKIN-1-BETA RELEASE; OXIDATIVE STRESS; INHIBITION; MACROPHAGES; APOPTOSIS; PATHOPHYSIOLOGY;
D O I
10.3892/mmr.2021.12153
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Sepsis is an imbalanced response to infection that leads to life-threatening organ dysfunction. Although an increasing number of anti-inflammatory drugs are available, the options for treating sepsis remain limited. Therefore, it is imperative to understand the pathogenesis and pathophysiology of sepsis and develop novel therapeutic targets to treat this state. The Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a cytoplasmic high-molecular weight protein complex composed of the sensor NLRP3, adapter protein apoptosis-related speck-like protein and pro-caspase-1. It functions by cleaving pro-caspase-1 to become active caspase-1, resulting in the maturation and release of IL-1 beta and IL-18. Activation of the NLRP3 inflammasome is necessary for innate immune defense and also serves an important role in adaptive immune responses. Studies have shown that the NLRP3 inflammasome is involved in the occurrence and evolution of sepsis and other immune inflammatory diseases. The present paper reviews the activation pathways and biological function of the NLRP3 inflammasome in sepsis, with the aim to provide a basis for further research.
引用
收藏
页数:8
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