The DOI matches its Crossref record; 153 of the 153 references it cites were found in a registry or an index.
Inflammasome Priming in Sterile Inflammatory Disease
Abstract
The inflammasome is a cytoplasmic protein complex that processes interleukins (IL)-1β and IL-18, and drives a form of cell death known as pyroptosis. Oligomerization of this complex is actually the second step of activation, and a priming step must occur first. This involves transcriptional upregulation of pro-IL-1β, inflammasome sensor NLRP3, or the non-canonical inflammasome sensor caspase-11. An additional aspect of priming is the post-translational modification of particular inflammasome constituents. Priming is typically accomplished in vitro using a microbial Toll-like receptor (TLR) ligand. However, it is now clear that inflammasomes are activated during the progression of sterile inflammatory diseases such as atherosclerosis, metabolic disease, and neuroinflammatory disorders. Therefore, it is time to consider the endogenous factors and mechanisms that may prime the inflammasome in these conditions.
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“The functional regulation of an active NLRP3 inflammasome in a cell is a ‘two-hit’ process, in which signal 1 primes the transcription of the inflammasome and signal 2, either by the same and/or additional stimuli, activates the inflammasome and induces secretion of two pro-inflammatory cytokines, IL-1β and IL-18 (REFS63,64).”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [63]
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2 retracted
RETRACTED: mTORC1-Induced HK1-Dependent Glycolysis Regulates NLRP3 Inflammasome Activation
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RetractedUCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis
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Self-citationNLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
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Cited by
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Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities
Bäck, M., Yurdagul, A., Tabas, I., Öörni, K., & Kovanen, P. T. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0169-2 · Cited by 1,341
Interleukin-1 Beta as a Target for Atherosclerosis Therapy
Libby, P. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.09.028 · Cited by 651
Mitochondrial Damage-Associated Molecular Patterns: From Inflammatory Signaling to Human Diseases
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Metadata
- Authors
- Patel, M. N., Carroll, R. G., Galván-Peña, S., Mills, E. L., Olden, R., Triantafilou, M., Wolf, A. I., Bryant, C. E., Triantafilou, K., & Masters, S. L.
- Affiliations
- GlaxoSmithKline (United Kingdom) (GB)
- GlaxoSmithKline (United States) (US)
- The University of Melbourne (AU)
- Corresponding author
- Masters, Seth L.
- ORCID
- Venue
- Trends in Molecular Medicine
- Publisher
- Elsevier BV
- Published
- 2017-02
- Volume
- 23
- Issue
- 2
- Pages
- 165-180
- ISSN
- 1471-4914 (ISSN-L)
- OpenAlex
- W2572287198
- Cited by
- 241
- References
- 153
- Citations by year
- 2026: 12 · 2025: 17 · 2024: 15 · 2023: 24 · 2022: 29 · 2021: 25 · 2020: 37 · 2019: 31 · 2018: 33 · 2017: 17
- FWCI
- 3.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- inflammasome priming, sterile inflammation, NLRP3 inflammasome, caspase-11, IL-1β processing, IL-18, pyroptosis, post-translational modification, atherosclerosis, metabolic disorders, neuroinflammation, Toll-like receptor ligands
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Alzheimer Disease, Animals, Humans, Immunity, Innate, Inflammation, Metabolic Diseases, Obesity, Neuroimmunomodulation, Atherosclerosis, Toll-Like Receptors, Interleukin-1beta, Hereditary Autoinflammatory Diseases, Inflammasomes
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