期刊
CELLULAR & MOLECULAR IMMUNOLOGY
卷 18, 期 9, 页码 2114-2127出版社
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/s41423-021-00740-6
关键词
NLRP3 inflammasome; pyroptosis; apoptosis; necroptosis; ferroptosis
类别
资金
- Fundamental Research Funds for the Central Universities [WK2070000191, WK9110000037]
- China National Postdoctoral Program for Innovative Talents [BX20200325]
- Natural Science Foundation of Anhui province [1808085QH244]
The NLRP3 inflammasome is a cytosolic multiprotein complex that responds to microbial infection, endogenous danger signals, and environmental stimuli. Its activation can induce pyroptosis and release of inflammatory cytokines, contributing to innate immune defense. However, aberrant activation of the NLRP3 inflammasome is associated with inflammatory diseases, and there is a close relationship between cell death pathways and NLRP3 inflammasome activation.
The NLRP3 inflammasome is a cytosolic multiprotein complex composed of the innate immune receptor protein NLRP3, adapter protein ASC, and inflammatory protease caspase-1 that responds to microbial infection, endogenous danger signals, and environmental stimuli. The assembled NLRP3 inflammasome can activate the protease caspase-1 to induce gasdermin D-dependent pyroptosis and facilitate the release of IL-1 beta and IL-18, which contribute to innate immune defense and homeostatic maintenance. However, aberrant activation of the NLRP3 inflammasome is associated with the pathogenesis of various inflammatory diseases, such as diabetes, cancer, and Alzheimer's disease. Recent studies have revealed that NLRP3 inflammasome activation contributes to not only pyroptosis but also other types of cell death, including apoptosis, necroptosis, and ferroptosis. In addition, various effectors of cell death have been reported to regulate NLRP3 inflammasome activation, suggesting that cell death is closely related to NLRP3 inflammasome activation. In this review, we summarize the inextricable link between NLRP3 inflammasome activation and cell death and discuss potential therapeutics that target cell death effectors in NLRP3 inflammasome-associated diseases.
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