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Cited by 322

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

ER stress activates the NLRP3 inflammasome via an UPR-independent pathway

Open access
Menu, P, Mayor, A, Zhou, R, Tardivel, A, Ichijo, H, Mori, K, Tschopp, J·2012·Cell Death & Disease

Abstract

Uncontrolled endoplasmic reticulum (ER) stress responses are proposed to contribute to the pathology of chronic inflammatory diseases such as type 2 diabetes or atherosclerosis. However, the connection between ER stress and inflammation remains largely unexplored. Here, we show that ER stress causes activation of the NLRP3 inflammasome, with subsequent release of the pro-inflammatory cytokine interleukin-1β. This ER-triggered proinflammatory signal shares the same requirement for reactive oxygen species production and potassium efflux compared with other known NLRP3 inflammasome activators, but is independent of the classical unfolded protein response (UPR). We thus propose that the NLRP3 inflammasome senses and responds to ER stress downstream of a previously uncharacterized ER stress response signaling pathway distinct from the UPR, thus providing mechanistic insight to the link between ER stress and chronic inflammatory diseases.

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Metadata

Authors
Menu, P., Mayor, A., Zhou, R., Tardivel, A., Ichijo, H., Mori, K., & Tschopp, J.
Venue
Cell Death & Disease
Published
2012-01-26
Volume
3
Issue
1
Pages
e261-e261
ISSN
2041-4889 (ISSN-L)
OpenAlex
W2059924886
Cited by
322
References
9
FWCI
11.73
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: ER stress activates the NLRP3 inflammasome via an UPR-independent pathway. https://app.cochat.ai/papers/10.1038/cddis.2011.132
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Menu, P., Mayor, A., Zhou, R., Tardivel, A., Ichijo, H., Mori, K., & Tschopp, J. (2012). ER stress activates the NLRP3 inflammasome via an UPR-independent pathway. Cell Death & Disease. https://doi.org/10.1038/cddis.2011.132

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