The DOI matches its Crossref record; 226 of the 226 references it cites were found in a registry or an index.
NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis
Abstract
Inflammation is an important driver of atherosclerosis, the underlying pathology of cardiovascular diseases. Therefore, therapeutic targeting of inflammatory pathways is suggested to improve cardiovascular outcomes in patients with cardiovascular diseases. This concept was recently proven by CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcomes Study), which demonstrated the therapeutic potential of the monoclonal IL (interleukin)-1β–neutralizing antibody canakinumab. IL-1β and other IL-1 family cytokines are important vascular and systemic inflammatory mediators, which contribute to atherogenesis. The NLRP3 (NOD [nucleotide oligomerization domain]-, LRR [leucine-rich repeat]-, and PYD [pyrin domain]-containing protein 3) inflammasome, an innate immune signaling complex, is the key mediator of IL-1 family cytokine production in atherosclerosis. NLRP3 is activated by various endogenous danger signals abundantly present in atherosclerotic lesions, such as oxidized low-density lipoprotein and cholesterol crystals. Consequently, NLRP3 inflammasome activation contributes to the vascular inflammatory response driving atherosclerosis development and progression. Here, we review the mechanisms of NLRP3 inflammasome activation and proinflammatory IL-1 family cytokine production in the context of atherosclerosis and discuss treatment possibilities in light of the positive outcomes of the CANTOS trial.
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“OxLDL has been shown both to prime and to activate the NLRP3 inflammasome in macrophages in mouse models of atherosclerosis: first, oxLDL primes the NLRP3 inflammasome by binding to the CD36–TLR4–TLR6 signalling complex on the macrophage surface and, then, after having been transported to lysosomes, the oxLDL activates the NLRP3 inflammasome via induction of cholesterol crystallization and ensuing”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [72]
In the citing paper
“Uptake of modified lipoproteins, such as oxLDL, has been shown in cultured macrophages to induce autophagy168, apoptosis170, pyroptosis (via induction of NRLP3 inflammasome activation72) and necroptosis169.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [72]
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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
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Metadata
- Authors
- Grebe, A., Hoss, F., & Latz, E.
- Affiliations
- University Hospital Bonn (DE)
- University of Massachusetts Chan Medical School (US)
- Venue
- Circulation Research
- Published
- 2018-06-08
- Volume
- 122
- Issue
- 12
- Pages
- 1722-1740
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2807678985
- Cited by
- 926
- References
- 226
- Citations by year
- 2026: 102 · 2025: 122 · 2024: 144 · 2023: 146 · 2022: 150 · 2021: 121 · 2020: 90 · 2019: 36 · 2018: 13
- FWCI
- 6.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- DZNE Pub (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL112661)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Keywords
- NLRP3 inflammasome, IL-1β, atherosclerosis, inflammation, canakinumab, CANTOS trial, innate immunity, oxidized LDL, cholesterol crystals, IL-1 family cytokines, atherogenesis, cardiovascular disease
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Antibodies, Monoclonal, Humans, Inflammation, Interleukin-1, Interleukin-6, Disease Progression, Interleukin-18, Atherosclerosis, Mice, Interleukin-1beta, Inflammasomes, Antibodies, Monoclonal, Humanized
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