Molecular mechanisms regulating NLRP3 inflammasome activation
Open accessAbstract
Inflammasomes are multi-protein signaling complexes that trigger the activation of inflammatory caspases and the maturation of interleukin-1β. Among various inflammasome complexes, the NLRP3 inflammasome is best characterized and has been linked with various human autoinflammatory and autoimmune diseases. Thus, the NLRP3 inflammasome may be a promising target for anti-inflammatory therapies. In this review, we summarize the current understanding of the mechanisms by which the NLRP3 inflammasome is activated in the cytosol. We also describe the binding partners of NLRP3 inflammasome complexes activating or inhibiting the inflammasome assembly. Our knowledge of the mechanisms regulating NLRP3 inflammasome signaling and how these influence inflammatory responses offers further insight into potential therapeutic strategies to treat inflammatory diseases associated with dysregulation of the NLRP3 inflammasome.
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ATP may act as a DAMP, which activates the nuclear transcription factor NF-κB, resulting in expression upregulation of pro-IL-1β and pro-IL-18 and the NLRP3 protein.
“In these circumstances, ATP may act as DAMP, which activates the nuclear transcription factor NF-κB resulting in expression upregulation of pro-IL-1β and pro-IL-18 and the NLRP3 protein [16, 71].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [71]
Consequently, there is an activation of caspase-1 and maturation of IL-1β and IL-18, resulting in pro-inflammatory cytokine release.
“Consequently, there is an activation of caspase-1 and maturation of IL-1β and IL-18, resulting in pro-inflammatory cytokine release [16, 20, 52, 71, 73].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [71]
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Cellular and molecular regulation of innate inflammatory responses
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Transplantation and Damage-Associated Molecular Patterns (DAMPs)
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The P2X7 Receptor: Central Hub of Brain Diseases
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Strategies for Targeting the NLRP3 Inflammasome in the Clinical and Preclinical Space
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TLRs/NLRs: Shaping the landscape of host immunity
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Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology
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Microglial inflammation and phagocytosis in Alzheimer's disease: Potential therapeutic targets
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Glial Contribution to Excitatory and Inhibitory Synapse Loss in Neurodegeneration
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Stress-induced NLRP3 inflammasome activation negatively regulates fear memory in mice
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Cell death in chronic inflammation: breaking the cycle to treat rheumatic disease
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Echinatin effectively protects against NLRP3 inflammasome–driven diseases by targeting HSP90
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Mitochondria as a target for neuroprotection: role of methylene blue and photobiomodulation
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NLRP3 inflammasome: a key player in the pathogenesis of life-style disorders
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New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation
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Mitochondria as a centrally positioned hub in the innate immune response
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Bacteroides fragilis restricts colitis-associated cancer via negative regulation of the NLRP3 axis
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Mechanisms of immune response to inorganic nanoparticles and their degradation products
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Fluoxetine Inhibits NLRP3 Inflammasome Activation: Implication in Depression
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New Insights into the Mechanisms of Pyroptosis and Implications for Diabetic Kidney Disease
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Crosstalk Between Dysfunctional Mitochondria and Inflammation in Glaucomatous Neurodegeneration
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Bergapten inhibits NLRP3 inflammasome activation and pyroptosis via promoting mitophagy
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AIM2 Inflammasome Is Critical for Influenza-Induced Lung Injury and Mortality
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Pannexin1 as mediator of inflammation and cell death
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- Authors
- Jo, E.-K., Kim, J. K., Shin, D.-M., & Sasakawa, C.
- Affiliations
- Chungnam National University (KR)
- Chiba University (JP)
- Corresponding author
- Jo, Eun-Kyeong
- Venue
- Cellular & Molecular Immunology
- Published
- 2015-11-09
- Volume
- 13
- Issue
- 2
- Pages
- 148-159
- ISSN
- 1672-7681 (ISSN-L)
- 2042-0226
- PMC
- PMC4786634
- OpenAlex
- W2118918019
- Cited by
- 1,378
- References
- 139
- Citations by year
- 2026: 127 · 2025: 125 · 2024: 157 · 2023: 162 · 2022: 145 · 2021: 173 · 2020: 171 · 2019: 122 · 2018: 97 · 2017: 61 · 2016: 36
- FWCI
- 6.27
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Cellular and Molecular Immunology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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
- NLRP3 inflammasome, inflammasome activation, caspase-1, autoinflammatory disease, autoimmune disease, anti-inflammatory therapy, inflammasome assembly, inflammatory diseases
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Autoimmune Diseases, Cytosol, Humans, Inflammation, Signal Transduction, Interleukin-1beta, Inflammasomes
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