Journal
APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
Volume 104, Issue 14, Pages 6129-6140Publisher
SPRINGER
DOI: 10.1007/s00253-020-10614-y
Keywords
Endoplasmic reticulum stress; NLRP3 inflammasome; Inflammation; Reactive oxygen species; NF-kappa B
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Funding
- National Natural Science Foundation of China [81201331]
- Major special projects of the Hunan Provincial Health and Family Planning Commission [A2017011]
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Endoplasmic reticulum stress (ERS) is a protective response to restore protein homeostasis by activating the unfolded protein response (UPR). However, UPR can trigger cell death under severe and/or persistently high ERS. The NLRP3 inflammasome is a complex of multiple proteins that activates the secretion of the proinflammatory cytokine IL-1 beta in a caspase-1-dependent manner to participate in the regulation of inflammation. The NLRP3 inflammasome involvement in ERS-induced inflammation has not been completely described. The intersection of ERS with multiple inflammatory pathways can initiate and aggravate chronic diseases. Accumulating evidence suggests that ERS-induced activation of NLRP3 inflammasome is the pathological basis of various inflammatory diseases. In this review, we have discussed the networks between ERS and NLRP3 inflammasome, with the view to identifying novel therapeutic targets in inflammatory diseases.
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