ReviewClinical & translational immunology2022
Inflammasome activation: from molecular mechanisms to autoinflammation.
Review in Clinical & translational immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 55 citations in OpenAlex.
- Decode the Ubiquitinome in Parkinson's Disease: From Pathological Aggregates to Targeted DUB Therapeutics.Neuroscience bulletin · 2026Review
- Article
- Inflammatory signatures in the spectrum of myeloid diseases.HemaSphere · 2026Article
- Article
- The Role of NLRP1, AIM2 and MEFV Inflammasomes in the High-Intensity Interval Training of Individuals With Obesity.Immunology · 2026Article
- Heterozygous NFKB1 variant causes inflammatory dysregulation shaped by broader genetic context in common variable immunodeficiency.JCI insight · 2026Article
- The Intracellular C5a-mtC5aR1 Axis Promotes Necroptosis in Dry Eye Through DRP1-Mediated Mitochondrial Dysfunction.Investigative ophthalmology & visual science · 2026Article
- Gut microbiota-cancer crosstalk: emerging molecular targets for personalized cancer treatment- a comprehensive review.Frontiers in molecular biosciences · 2026Review
- Beyond a gatekeeper: the non-classical signaling role of STRA6 in driving endothelial senescence and atherosclerosis.Frontiers in immunology · 2026Review
- An animal model of NLRC4-associated autoinflammation and infantile enterocolitis reveals novel therapeutic strategies.Cellular & molecular immunology · 2025Article
- circRNA/TLR interaction: key players in immune regulation and autoimmune diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Review
- The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- Effect of Vitamin D3 on the Levels of Oxidative Stress and Expression of the NLRP3 Inflammatory Gene in Type 2 Diabetes Mellitus: A Randomized Clinical Trial.Health science reports · 2025Article
- Differential expression ofVeterinary world · 2025Article
- Non-coding RNAs affecting NLRP3 inflammasome pathway in diabetic cardiomyopathy: a comprehensive review of potential therapeutic options.Journal of translational medicine · 2025Review
- Targeting Ferroptosis/Nrf2 Pathway Ameliorates AlClInternational journal of molecular sciences · 2025Article
- FACS-based detection of extracellular ASC specks from NLRP3 inflammasomes in inflammatory diseases.Clinical and experimental immunology · 2025Article
- CMPK2 promotes NLRP3 inflammasome activation via mtDNA-STING pathway in house dust mite-induced allergic rhinitis.Clinical and translational medicine · 2025Article
- Autophagy and inflammasome activation are associated with poor response to FLT3 inhibitors in patients with FLT3-ITD acute myeloid leukemia.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasomes are assembled by innate immune sensors that cells employ to detect a range of danger signals and respond with pro-inflammatory signalling. Inflammasomes activate inflammatory caspases, which trigger a cascade of molecular events with the potential to compromise cellular integrity and release the IL-1β and IL-18 pro-inflammatory cytokines. Several molecular mechanisms, working in concert, ensure that inflammasome activation is tightly regulated; these include NLRP3 post-translational modifications, ubiquitination and phosphorylation, as well as single-domain proteins that competitively bind to key inflammasome components, such as the CARD-only proteins (COPs) and PYD-only proteins (POPs). These diverse regulatory systems ensure that a suitable level of inflammation is initiated to counteract any cellular insult, while simultaneously preserving tissue architecture. When inflammasomes are aberrantly activated can drive excessive production of pro-inflammatory cytokines and cell death, leading to tissue damage. In several autoinflammatory conditions, inflammasomes are aberrantly activated with subsequent development of clinical features that reflect the degree of underlying tissue and organ damage. Several of the resulting disease complications may be successfully controlled by anti-inflammatory drugs and/or specific cytokine inhibitors, in addition to more recently developed small-molecule inhibitors. In this review, we will explore the molecular processes underlying the activation of several inflammasomes and highlight their role during health and disease. We also describe the detrimental effects of these inflammasome complexes, in some pathological conditions, and review current therapeutic approaches as well as future prospective treatments.
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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.