Literature DB >> 32058297

TRPM2, linking oxidative stress and Ca2+ permeation to NLRP3 inflammasome activation.

Longfei Wang1, Roberto Negro1, Hao Wu2.   

Abstract

The NLRP3 inflammasome is an innate immune platform that senses various pathogens and sterile insults. NLRP3 stimulation leads to activation of caspase-1, the secretion of pro-inflammatory cytokines and an inflammatory cell death called pyroptosis. Effectors of the NLRP3 inflammasome efficiently drive an immune response, not only providing protection in physiological settings but also promoting pathology when over activated. Generation of reactive oxygen species (ROS) and intracellular calcium mobilization can activate the NLRP3 inflammasome. Recent studies suggest that TRPM2 is a calcium-permeable cation channel mediating ROS-dependent NLRP3 activation. Here, we review the role of TRPM2 in NLRP3 inflammasome activation and provide an update on new functional and structural discoveries. Understanding the molecular mechanism of TRPM2 dependent NLRP3 inflammasome activation will shed lights on this complex pathway and help the developing of therapeutic strategies.
Copyright © 2020 Elsevier Ltd. All rights reserved.

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Year:  2020        PMID: 32058297      PMCID: PMC7533107          DOI: 10.1016/j.coi.2020.01.005

Source DB:  PubMed          Journal:  Curr Opin Immunol        ISSN: 0952-7915            Impact factor:   7.486


  37 in total

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6.  Purinergic signaling elements are correlated with coagulation players in peripheral blood and leukocyte samples from COVID-19 patients.

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Review 10.  Synergistic Impairment of the Neurovascular Unit by HIV-1 Infection and Methamphetamine Use: Implications for HIV-1-Associated Neurocognitive Disorders.

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