The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
Endoplasmic Reticulum Stress Activates the Inflammasome via NLRP3- and Caspase-2-Driven Mitochondrial Damage
Open accessAbstract
SUMMARY Endoplasmic reticulum (ER) stress is observed in many human diseases, often associated with inflammation. ER stress can trigger inflammation through nucleotide-binding domain and leucine-rich repeat containing (NLRP3) inflammsome, which may stimulate inflammasome formation by association with damaged mitochondria. How ER stress triggers mitochondrial dysfunction and inflammasome activation is ill defined. Here we have used an infection model to show that the IRE1α ER stress sensor regulates regulated mitochondrial dysfunction through an NLRP3-mediated feed-forward loop, independently of ASC. IRE1α activation increased mitochondrial reactive oxygen species, promoting NLRP3 association with mitochondria. NLRP3 was required for ER stress-induced cleavage of caspase-2 and the pro-apoptotic factor, Bid, leading to subsequent release of mitochondrial contents. Caspase-2 and Bid were necessary for activation of the canonical inflammasome by infection-associated or general ER stress. These data identify an NLRP3-caspase-2 dependent mechanism that relays ER stress to the mitochondria to promote inflammation, integrating cellular stress and innate immunity.
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Cites
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Self-citationThioredoxin-interacting protein links oxidative stress to inflammasome activation
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Cited by
Mechanisms, regulation and functions of the unfolded protein response
Hetz, C., Zhang, K., & Kaufman, R. J. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0250-z · Cited by 2,666
Reactive Oxygen Species in Metabolic and Inflammatory Signaling
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Protein misfolding in the endoplasmic reticulum as a conduit to human disease
Wang, M., & Kaufman, R. J. (2016) · Nature · doi:10.1038/nature17041 · Cited by 1,630
Mitochondrial DNA in innate immune responses and inflammatory pathology
West, A. P., & Shadel, G. S. (2017) · Nature Reviews Immunology · doi:10.1038/nri.2017.21 · Cited by 1,115
The role of mitochondria in NLRP3 inflammasome activation
Liu, Q., Zhang, D., Hu, D., Zhou, X., & Zhou, Y. (2018) · Molecular Immunology · doi:10.1016/j.molimm.2018.09.010 · Cited by 475
Metadata
- Authors
- Bronner, D. N., Abuaita, B. H., Chen, X., Fitzgerald, K. A., Nuñez, G., He, Y., Yin, X.-M., & O’Riordan, M. X. D.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2015-09
- Volume
- 43
- Issue
- 3
- Pages
- 451-462
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2149766325
- Cited by
- 437
- References
- 58
- FWCI
- 14.15
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Bronner, D. N., Abuaita, B. H., Chen, X., Fitzgerald, K. A., Nuñez, G., He, Y., Yin, X.-M., & O’Riordan, M. X. D. (2015). Endoplasmic Reticulum Stress Activates the Inflammasome via NLRP3- and Caspase-2-Driven Mitochondrial Damage. Immunity. https://doi.org/10.1016/j.immuni.2015.08.008
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