ArticleFrontiers in immunology2025
Gas6 induces AIM to suppress acute lung injury in mice by inhibiting NLRP3 inflammasome activation and inducing autophagy.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Sulfhydrated TFEB alleviates blast-induced lung injury by maintaining epithelial barrier integrity through the IGF2R/MMP-2/9 pathway.Redox biology · 2026Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Electroacupuncture in the treatment of non-alcoholic fatty liver disease: mechanistic insights and therapeutic potential.Frontiers in medicine · 2026Review
- Heterogeneity of Lung Phagocytes and Clearance of Apoptotic Cells in Lung Injury and Repair.Seminars in respiratory and critical care medicine · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Growth arrest-specific 6 (Gas6) protein signaling plays a critical role in maintaining immune homeostasis and regulating inflammation. However, novel mechanisms for modulating macrophage activity through the Gas6 axis are being identified. Gas6 enhances the production of apoptosis inhibitor of macrophages (AIM), a protein with potent anti-inflammatory properties. This study investigates whether Gas6-induced AIM suppresses acute lung injury (ALI) in mice by modulating key inflammatory pathways, including inflammasome activation, autophagy, reactive oxygen species (ROS) generation, and efferocytosis. Methods: ALI was induced in wild-type (WT) and Results: Proinflammatory cytokine production, neutrophil infiltration, and protein levels in BALF were significantly reduced by rGas6 administration in WT mice but not in Conclusion: Gas6-induced AIM production protects against LPS-induced ALI by inhibiting NLRP3 inflammasome activation, enhancing autophagy and efferocytosis, and reducing oxidative stress. These findings highlight the Gas6-AIM axis as a potential therapeutic target for mitigating inflammatory lung diseases.
Indexed as
Identifiers
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.