ReviewClinical and translational medicine2024
The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome.
Review in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- TRPV4 drives macrophage pyroptosis via mitochondrial dysfunction and mtROS-dependent NLRP3 inflammasome activation in acute lung injury.Redox biology · 2026Article
- Beyond Supportive Care: Mitochondria as a Strategic Therapeutic Avenue in Acute Pancreatitis.Digestive diseases and sciences · 2026Review
- GPR161 contributes to macrophage glycolytic reprogramming via targeting C5aR1 in acute lung injury.Cellular & molecular biology letters · 2026Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Precision immunomodulation of viral myocarditis: a spatiotemporal intervention paradigm based on smart biomaterials.Frontiers in immunology · 2026Review
- Inhalable songorine-integrated lipid nanomedicine for targeted ARDS therapyActa pharmaceutica Sinica. B · 2026Article
- Macrophage Hypoxia Signaling Pathways and Their Roles in Sepsis.Journal of inflammation research · 2026Review
- Article
- Cell-specific exosomes in sepsis-associated ARDS: from immunometabolic reprogramming to precision medicine.Frontiers in immunology · 2026Review
- Metabolite-neuro-immune relay in chronic pain: spatial-temporal lactate, succinate and itaconate signalling as drivers of glial reprogramming and neuronal sensitisation.Frontiers in pharmacology · 2026Review
- Mitochondrial dysfunction in ARDS: unraveling the regulatory networks and therapeutic opportunities.Frontiers in immunology · 2026Review
- Advances in natural product-based nanoparticles for the treatment of acute lung injury.Materials today. Bio · 2025Review
- Article
- Novel Triazine Derivatives as NLRP3 Inhibitors for Treating Asthma or COPD.ACS medicinal chemistry letters · 2025Article
- P2Y12R Blockade Attenuates LPS-Induced Acute Lung Injury Associated with Suppression of Inflammasome-Mediated Pyroptotic Signaling.Drug design, development and therapy · 2025Article
- Macrophage polarization: molecular mechanisms, disease implications, and targeted therapeutic strategies.Frontiers in immunology · 2025Review
- Multi-Omics and Clinical Validation Identify Key Glycolysis- and Immune-Related Genes in Sepsis.International journal of general medicine · 2025Article
- Decoding immune-metabolic crosstalk in ARDS: a transcriptomic exploration of biomarkers, cellular dynamics, and therapeutic pathways.Frontiers in immunology · 2025Article
- The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome.Clinical and translational medicine · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe respiratory condition associated with elevated morbidity and mortality. Understanding their complex pathophysiological mechanisms is crucial for developing new preventive and therapeutic strategies. Recent studies highlight the significant role of inflammation involved in ALI/ARDS, particularly the hyperactivation of the NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome in macrophages. This activation drives pulmonary inflammation by releasing inflammatory signalling molecules and is linked to metabolic reprogramming, marked by increased glycolysis and reduced oxidative phosphorylation. However, the relationship between NLRP3 inflammasome activation and macrophage glycolytic reprogramming in ALI/ARDS, as well as the molecular mechanisms regulating these processes, remain elusive. This review provides a detailed description of the interactions and potential mechanisms linking NLRP3 inflammasome activation with macrophage glycolytic reprogramming, proposing that glycolytic reprogramming may represent a promising therapeutic target for mitigating inflammatory responses in ALI/ARDS. KEY POINTS: NLRP3 inflammasome activation is pivotal in mediating the excessive inflammatory response in ALI/ARDS. Glycolytic reprogramming regulates NLRP3 inflammasome activation. Therapeutic potential of targeting glycolytic reprogramming to inhibit NLRP3 inflammasome activation in ALI/ARDS.
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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.