Abstract
Inflammasomes, multiprotein complex induced by harmful factors in the body, play a crucial role in innate immunity. Activation of inflammasomes lead to the activation of casepase-1 and then the secretion of inflammatory cytokines, including IL-1β and IL-18, subsequently leading to a type of cell death called pyroptosis. There are two types of signaling pathways involved in the process of inflammasome activation: the canonical and the non-canonical signaling pathway. The canonical signaling pathway is mainly dependent on casepase-1; the non-canonical signal pathway, which was recently discovered, is mainly dependent on caspase-11, but is also meditated by caspase-4, caspase-5, and caspase-8. Kidney inflammation is basically associated with inflammatory factor exudation and inflammatory cell infiltration. Several studies have showed that inflammasomes are closely related to kidney diseases, especially the NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome, which play a role in regulating kidney inflammation and fibrosis. In this review, we focus on the relationship between inflammasomes and kidney diseases, especially the role of the NLRP3 inflammasome in different kinds of kidney disease via both canonical and non-canonical signal pathways.
Highlights
Inflammasomes are sensors of innate immunity that are triggered in response to danger signals
The NLRP3 inflammasome is an intermediate medium for the rapid response of the body to the external injury, including activation of inflammatory cytokine and pyroptotic cell death
Inflammasomes play a different role in various diseases, and mainly induce the inflammation and dysfunction of kidney; interfering the process of NLRP3 inflammasome activation can regulate the kidney injury
Summary
Inflammasomes are sensors of innate immunity that are triggered in response to danger signals. In the presence of a signal, the PAMPs or DAMPs activate the PRRs on NLRs or TLRs, which triggers the ASC adaptor to activate the effector caspase-1 or caspase-11 The activation of these molecules can lead to the secretion of proinflammatory cytokine pro-IL-1β, pro-IL-18 as well as the cleavage of gasdermin D (GSDMD), thereby triggering cell pyroptosis (Conforti-Andreoni et al, 2011; Kayagaki et al, 2011; Kovacs and Miao, 2017). The canonical pathway involving caspase-1 has been highly researched; the role and underlying mechanism of the inflammasomes, involving caspase-11 or other effectors like caspase-4, caspase-5, and caspase-8, which were recently identified to be part of a non-canonical signaling pathway, remains poorly understood (Gurung et al, 2014; Vigano et al, 2015) Depending on their differences in structure and activation, the inflammasomes are divided into NLRP1, NOD-, LRR- and pyrin domain-containing 3 (NLRP3), NLRC4, IPAF, and AIM2 inflammasomes (de Zoete et al, 2014). Inflammasome might be a potential target in the treatment of renal disease, suggesting development of novel effective therapeutics for kidney diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
