ReviewImmunological reviews2015
Inhibiting the inflammasome: one domain at a time.
Review in Immunological reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Importance of the inflammasome in gut-brain axis: from pathological driver to therapeutic target.Inflammopharmacology · 2026Review
- NLR Inflammasomes in Viral Infections: From Molecular Mechanisms to Therapeutic Interventions.Viruses · 2026Review
- The ASC-c isoform as a modulator of inflammasome activation: Insights into molecular mechanisms and therapeutic applications.The Journal of biological chemistry · 2026Article
- The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities.MedComm · 2026Review
- Article
- Irisin Attenuates Neuroinflammation Targeting the NLRP3 Inflammasome.Molecules (Basel, Switzerland) · 2024Article
- Oligomeric states of ASC specks regulate inflammatory responses by inflammasome in the extracellular space.Cell death discovery · 2023Article
- Does Pyroptosis Play a Role in Inflammasome-Related Disorders?International journal of molecular sciences · 2022Review
- Inflammasome activation: from molecular mechanisms to autoinflammation.Clinical & translational immunology · 2022Review
- NLRP7: From inflammasome regulation to human disease.Immunology · 2021Review
- Great balls of fire: activation and signalling of inflammatory caspases.Biochemical Society transactions · 2021Review
- Article
- Functions of ROS in Macrophages and Antimicrobial Immunity.Antioxidants (Basel, Switzerland) · 2021Review
- Role of Pyroptosis in Diabetes and Its Therapeutic Implications.Journal of inflammation research · 2021Review
- Review
- An overview of the non-canonical inflammasome.Molecular aspects of medicine · 2020Review
- Immunobiology and structural biology of AIM2 inflammasome.Molecular aspects of medicine · 2020Review
- Fructose-arginine, a non-saponin molecule of Korean Red Ginseng, attenuates AIM2 inflammasome activation.Journal of ginseng research · 2020Review
- Emerging role of IL-6 and NLRP3 inflammasome as potential therapeutic targets to combat COVID-19: Role of lncRNAs in cytokine storm modulation.Life sciences · 2020Review
- The Emerging Relevance of AIM2 in Liver Disease.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Inflammasomes are protein complexes that promote the maturation and release of pro-inflammatory cytokines and danger signals as well as pyroptosis in response to infections and cellular stress. Inflammasomes consist of a sensor, an adapter, and the effector caspase-1, which interact through homotypic interactions of caspase recruitment domains (CARDs) or PYRIN domains (PYDs). Hence, decoy proteins encoding only a CARD or PYD, COPs and POPs, respectively, are assumed to inhibit inflammasome assembly. Sensors encoding a PYD belong to the families of NOD-like receptors containing a PYD (NLRPs) or AIM2-like receptors (ALRs), which interact with the PYD- and CARD-containing adapter ASC through homotypic PYD interactions. Subsequently, ASC undergoes PYD-dependent oligomerization, which promotes CARD-mediated interactions between ASC and caspase-1, resulting in caspase-1 activation. POPs are suggested to interfere with the interaction between NLRPs/ALRs and ASC to prevent nucleation of ASC and therefore prevent an oligomeric platform for caspase-1 activation. Similarly, COPs are suggested to bind to the CARD of caspase-1 to prevent its recruitment to the oligomeric ASC platform and its activation. Alternatively, the adapter ASC may regulate inflammasome activity by expressing different isoforms, which are either capable or incapable of assembling an oligomeric ASC platform. The molecular mechanism of inflammasome assembly has only recently been elucidated, but the effects of most COPs and POPs on inflammasome assembly have not been investigated. Here, we discuss our model of COP- and POP-mediated inflammasome regulation.
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Registered trials
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.