期刊
JOURNAL OF AUTOIMMUNITY
卷 113, 期 -, 页码 -出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jaut.2020.102515
关键词
NLRP3 inflammasome; NEK7; Activation mechanism; NLRP3 inflammasome inhibitor; NLRP3-Driven disease
类别
资金
- National Natural Science Foundation of China [81803354, 81773693, 2018YFC0807402]
- National Key R&D Program of China [BK20180564]
- Natural Science Foundation of Jiangsu Province of China [2017M620232]
- China Postdoctoral Science Foundation [CPU2018GY02]
- Double First Class Innovation Team of China Pharmaceutical University
The nucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin domain 3 (NLRP3) inflammasome is a high-molecular-weight complex mediated by the activation of pattern-recognition receptors (PRRs) seed in innate immunity. Once NLRP3 is activated, the following recruitment of the adapter apoptosisassociated speck-like protein containing a caspase recruitment domain (CARD) (ASC) and procaspase-1 would be initiated. Cleavage of procaspase-1 into active caspase-1 then leads to the maturation of the precursor forms of interleukin (IL)-1 beta and IL-18 into biologically active IL-1 beta and IL-18. The activation of NLRP3 inflammasome is thought to be tightly associated with a regulator never in mitosis A (NIMA)-related kinase 7 (NEK7), apart from other signaling events such as K+ efflux and reactive oxygen species (ROS). Plus, the NLRP3 inflammasome has been linked to various metabolic disorders, chronic inflammation and other diseases. In this review, we firstly describe the cellular/molecular mechanisms of the NEK7-licensed NLRP3 inflammasome activation. Then we detail the potential inhibitors that can selectively and effectively modulate either the NEK7-NLRP3 complex itself or the related molecular/cellular events. Finally, we describe some inhibitors as promising therapeutic strategies for diverse diseases driven by NLRP3 inflammasome.
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