ReviewThorax2025
Role of inflammasomes in acute respiratory distress syndrome.
Review in Thorax, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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
15 citing papers in PubMed.
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Diffuse alveolar damage, acute respiratory distress syndrome (ARDS), and non-cardiogenic pulmonary edema (NCPE). Part 2: NCPE apart from ARDS, molecular and cellular consequences of primary injury to the lung interstitium, with comparative immunology of the dog and cat.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2026Review
- GBP5 Aggravates Acute Lung Injury Via NLRP3 Inflammasome Activation While Inducing a HIF-1α-CD73-adenosine Feedback Loop.Inflammation · 2026Article
- IL-1β modulates inflammatory response of human bone marrow-derived MSCs and neutrophil recruitment in vitro via NF-kB-associated signaling.Stem cell research & therapy · 2026Article
- When Infection Meets Inflammation:Biology · 2026Review
- Mapping the Ischemic Continuum: Dynamic Multi-Omic Biomarker and AI for Personalized Stroke Care.International journal of molecular sciences · 2026Review
- The Role of Alpha-1 Antitrypsin in the Pathophysiology and Treatment of Inflammatory Lung Diseases.Journal of inflammation research · 2026Review
- NLRP3 inflammasomes at the ARDS-cancer interface: mechanisms and translational hypotheses.Frontiers in immunology · 2026Review
- Celastrol-Based Hybrid Prodrug Ameliorates ALI by Spatiotemporally Consecutive Dual-Targeting GLUT1/Drp1 to Reestablish Mitochondrial Homeostasis.International journal of biological sciences · 2026Article
- Regulation of neutrophil function by the extracellular matrix.Biochemical Society transactions · 2025Review
- Acute Respiratory Distress Syndrome: Pathophysiological Insights, Subphenotypes, and Clinical Implications-A Comprehensive Review.Journal of clinical medicine · 2025Review
- Immunomodulatory therapies in community-acquired pneumonia: a protocol for a systematic review and network meta-analysis.BMJ open · 2025Article
- Experimental animal models of acute respiratory distress syndrome: one-hit and two-hit establishment application.Frontiers in immunology · 2025Review
- Association Between Heparin-Binding Protein and Extubation Outcomes in ARDS: A Retrospective Cohort Study.International journal of general medicine · 2025Article
- Targeting the NLRP3-ROS Axis: Disrupting the Oxidative-Inflammatory Vicious Cycle in Intracerebral Hemorrhage.Journal of inflammation research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute respiratory distress syndrome (ARDS) is present in >10% of all people admitted to critical care and is associated with severe morbidity and mortality. Despite more than half a century since its first description, no efficacious pharmacological therapies have been developed, and little progress has been made in improving clinical outcomes. Neutrophils are the principal drivers of ARDS, with their priming and subsequent aberrant downstream functions, including interleukin (IL) 1β and IL-18 secretion, central to the disease pathogenesis. The dominant pathways through which IL-1β and IL-18 are believed to be elaborated are multimeric protein structures called inflammasomes that consist of sensor proteins, adaptor proteins and an effector enzyme. The inflammasome's initial activation depends on one of a variety of damage-associated (DAMP) or pathogen-associated (PAMP) molecular patterns. However, once activated, a common downstream inflammatory pathway is initiated regardless of the specific DAMP or PAMP involved. Several inflammasomes exist in humans. The nucleotide-binding domain leucine-rich repeat (NLR) family, pyrin domain-containing 3 (NLRP3), inflammasome is the best described in the context of ARDS and is known to be activated in both infective and sterile cases. The NLR family, caspase activation and recruitment domain-containing 4 (NLRC4) and absent in melanoma 2 (AIM2) inflammasomes have also been implicated in various ARDS settings, as have inflammasome-independent pathways. Further work is required to understand human biology as much of our knowledge is extrapolated from rodent experimental models. Experimental lung injury models have demonstrated beneficial responses to inflammasome, IL-1β and IL-18 blockade. However, findings have yet to be successfully translated into humans with ARDS, likely due to an underappreciation of the central role of the neutrophil inflammasome. A thorough understanding of inflammasome pathways is vital for critical care clinicians and researchers and for the development of beneficial therapies. In this review, we describe the central role of the inflammasome in the development of ARDS and its potential for immunomodulation, highlighting key areas for future research.
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What Socratic holds
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 Socratic graph.