ReviewF1000Research2016
Recent insights into the molecular mechanisms of the NLRP3 inflammasome activation.
Review in F1000Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
94 citing papers in PubMed, 169 citations in OpenAlex.
- Article
- The mitophagy-inflammasome axis: a shared pathological hub in Alzheimer's and Parkinson's diseases.Translational neurodegeneration · 2026Review
- Time-lapse image analysis reveals trigger-dependent differences in ASC speck lifetime in the NLRP3 inflammasome.Scientific reports · 2026Article
- Tussilagone mitigates sepsis-induced acute lung injury in mice by suppressing RIPK1 expression.Hereditas · 2026Article
- TH5487 specifically targets NLRP3 in FCAS patients resistant to MCC950.Communications biology · 2026Article
- Qiming granules regulate Müller cell pyroptosis and the P2X7R/NLRP3 immune inflammatory pathway in diabetic retinopathy.Chinese medicine · 2026Article
- The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury.Journal of neuroinflammation · 2025Article
- The pH gradient contributes to persistence in Mycobacterium tuberculosis.Research square · 2025Article
- The role of maternal infections in neurodevelopmental psychiatric disorders: focus on the P2X7/NLRP3/IL-1β signalling pathway.Journal of neuroinflammation · 2025Review
- The key players of inflammasomes and pyroptosis in sepsis-induced pathogenesis and organ dysfunction.Frontiers in pharmacology · 2025Review
- Revealing the Mechanism of NLRP3 Inflammatory Pathway Activation through KInternational journal of molecular sciences · 2024Article
- Exposing kinetic disparities between inflammasome readouts using time-resolved analysis.Heliyon · 2024Article
- New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Exploring the role of IL-1β in inflammatory bowel disease pathogenesis.Frontiers in medicine · 2024Review
- Remote limb ischemic postconditioning inhibits microglia pyroptosis by modulating HGF after acute ischemia stroke.Bioengineering & translational medicine · 2023Article
- AR-A014418, a glycogen synthase kinase-3β inhibitor, mitigates lipopolysaccharide-induced inflammation in rat dental pulp stem cells via NLR family pyrin domain containing 3 inflammasome impairment.Journal of dental sciences · 2023Article
- Review
- ASC oligomer favors caspase-1CARD domain recruitment after intracellular potassium efflux.The Journal of cell biology · 2023Article
- Saponin-based adjuvants enhance antigen cross-presentation in human CD11cJournal for immunotherapy of cancer · 2023Article
- Immunohistochemical analysis of caspase expression in the brains of individuals with obesity or overweight.Obesity science & practice · 2023Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasomes are high-molecular-weight protein complexes that are formed in the cytosolic compartment in response to danger- or pathogen-associated molecular patterns. These complexes enable activation of an inflammatory protease caspase-1, leading to a cell death process called pyroptosis and to proteolytic cleavage and release of pro-inflammatory cytokines interleukin (IL)-1β and IL-18. Along with caspase-1, inflammasome components include an adaptor protein, ASC, and a sensor protein, which triggers the inflammasome assembly in response to a danger signal. The inflammasome sensor proteins are pattern recognition receptors belonging either to the NOD-like receptor (NLR) or to the AIM2-like receptor family. While the molecular agonists that induce inflammasome formation by AIM2 and by several other NLRs have been identified, it is not well understood how the NLR family member NLRP3 is activated. Given that NLRP3 activation is relevant to a range of human pathological conditions, significant attempts are being made to elucidate the molecular mechanism of this process. In this review, we summarize the current knowledge on the molecular events that lead to activation of the NLRP3 inflammasome in response to a range of K (+) efflux-inducing danger signals. We also comment on the reported involvement of cytosolic Ca (2+) fluxes on NLRP3 activation. We outline the recent advances in research on the physiological and pharmacological mechanisms of regulation of NLRP3 responses, and we point to several open questions regarding the current model of NLRP3 activation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.