| Literature DB >> 32081791 |
Dongling Liu1, Xiang Zeng2, Xiao Li3, Chaochu Cui3, Ruanling Hou4, Zhikun Guo3, Jawahar L Mehta5, Xianwei Wang6.
Abstract
NLRP3 inflammasome is an intracellular protein complex that initiates cellular injury via assembly of NLRP3, ASC and caspase-1 in response to microbial infection and sterile stressors. The importance of NLRP3 inflammasome in immunity and human diseases has been well documented. Up to now, targeted inhibition of the assembly of NLRP3 inflammasome complex and of its activation was thought to be therapeutic strategy for associated diseases. Recent studies show that a host of molecules such as NIMA-related kinase 7 (Nek7) and DEAD-box helicase 3 X-linked (DDX3X) and a large number of biological mediators including cytokines, microRNAs, nitric oxide, carbon monoxide, nuclear factor erythroid-2 related factor 2 (Nrf2) and cellular autophagy participate in the activation and inactivation of NLRP3 inflammasome. This review summarizes current understanding of the molecular basis of NLRP3 inflammasome activation and inactivation. This knowledge may lead to development of new therapies directed at NLRP3 inflammasome related diseases.Entities:
Keywords: DEAD-box helicase 3 X-linked; Interleukin-1β; NIMA-related kinase 7; NLRP3 inflammasome; Therapeutic target
Year: 2020 PMID: 32081791 DOI: 10.1016/j.bcp.2020.113863
Source DB: PubMed Journal: Biochem Pharmacol ISSN: 0006-2952 Impact factor: 5.858