ReviewInternational journal of molecular sciences2024
NLRP3 Inflammasome in Acute and Chronic Liver Diseases.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Protective effects ofRedox report : communications in free radical research · 2026Article
- Loganin Alleviates CClChinese journal of integrative medicine · 2026Article
- The NLRP3 inflammasome as a dynamic context-dependent regulator: mechanisms, disease progression, and therapeutic implications.Journal of translational medicine · 2026Review
- USP9X regulates copper-induced CASP9/CASP3/GSDME-dependent pyroptosis by deubiquitinating JAK1.Apoptosis : an international journal on programmed cell death · 2026Article
- Micro- and Nanoplastics as Emerging Drivers of Liver Injury: Exposure, Evidence, and Mechanisms.International journal of molecular sciences · 2026Review
- Chronic Intermittent Hypoxia Exacerbates High-Fat Diet-Induced MASLD Through Lipid Metabolic Reprogramming, Impaired Antioxidant Defense, and NF-κB/NLRP3 Activation.Biomolecules · 2026Article
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Thioredoxin-Binding protein 2 and apoptosis Signal-Regulating kinase 1: redox stress sensors and therapeutic targets in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- NLRP3/Caspase-1 Regulate Macrophage Efferocytosis by Modulating ADAM17-Mediated MerTK Cleavage in Liver Ischemia-Reperfusion Injury.Research (Washington, D.C.) · 2026Article
- Bioactive compounds as therapeutic modulators of metabolic syndrome: targeting inflammation and gut microbiota regulation.Frontiers in physiology · 2026Review
- Article
- Targeting inflammatory dysregulation in metabolic dysfunction-associated steatotic liver disease rat model: the preventive and therapeutic effects of acetyl-11-keto-beta-boswellic acid.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Protective Effects of Resveratrol on Heat Stress-Induced Liver Dysfunction in Broilers Through Modulating Autophagy and NLRP3 Inflammasome.Food science & nutrition · 2025Article
- How interactions between oxidized DNA and the NLRP3 inflammasome fuel inflammatory disease.Trends in biochemical sciences · 2025Review
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- Macrophages: Subtypes, Distribution, Polarization, Immunomodulatory Functions, and Therapeutics.MedComm · 2025Review
- NLRP3 inflammasome: structure, mechanism, drug-induced organ toxicity, therapeutic strategies, and future perspectives.RSC medicinal chemistry · 2025Review
- Effects of remote ischemic preconditioning and/or erythropoietin on lung injury induced by skeletal ischemia reperfusion: role of the NLRP3 inflammasome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- NLRP3 as a therapeutic target in cyclophosphamide-associated toxicities.Molecular biology reports · 2025Review
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) is an intracellular complex that upon external stimuli or contact with specific ligands, recruits other components, forming the NLRP3 inflammasome. The NLRP3 inflammasome mainly mediates pyroptosis, a highly inflammatory mode of regulated cell death, as well as IL-18 and IL-1β production. Acute and chronic liver diseases are characterized by a massive influx of pro-inflammatory stimuli enriched in reactive oxygen species (ROS) and damage-associated molecular patterns (DAMPs) that promote the assemblage and activation of the NLRP3 inflammasome. As the major cause of inflammatory cytokine storm, the NLRP3 inflammasome exacerbates liver diseases, even though it might exert protective effects in regards to hepatitis C and B virus infection (HCV and HBV). Here, we summarize the current knowledge concerning NLRP3 inflammasome function in both acute and chronic liver disease and in the post liver transplant setting, focusing on the molecular mechanisms involved in NLRP3 activity.
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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.