ArticleImmunity, inflammation and disease2025
The Protective Effects of Annexin A1 in Acute Lung Injury Mediated by Nrf2.
Article in Immunity, inflammation and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Annexin A1 and Dexamethasone Treatment in Hospitalized COVID-19 Patients: Impact on Disease Recovery and Evidence for an Interplay Between Proresolving Mediators.Biomolecules · 2026Article
- High-Altitude Hypoxic Preconditioning Attenuates Lipopolysaccharide-Induced Lung Injury and is Associated with Alveolar-Capillary Barrier Maintenance.Journal of inflammation research · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
backgroundAcute lung injury (ALI), one of the most severe respiratory system diseases, is prevalent worldwide. Annexin A1 (AnxA1) is an important member of the annexin superfamily, known for its wide range of physiological functions. However, its potential protective effect against lipopolysaccharide (LPS)-induced ALI remains unclear. MATERIALS AND
methodsMice were divided into four groups: Sham, LPS + vehicle, LPS + 0.1 μg AnxA1, and LPS + 0.5 μg AnxA1. Lung injury was assessed through histopathology, pulmonary wet-to-dry (W/D) ratio, cell counting of bronchoalveolar lavage fluid (BALF), oxidative stress analysis, and noninvasive pulmonary function testing. Gene and protein expression levels were measured using RT-PCR, ELISA, and western blot analysis.
resultsAnxA1 alleviated LPS-induced ALI by protecting lung tissue from damage, reducing the lung wet/dry (W/D) weight ratio, and improving LPS-induced impaired lung function. Interestingly, administration of AnxA1 was found to repress the infiltration of inflammatory cells by decreasing the total cell count, neutrophils, and protein concentrations in bronchoalveolar lavage fluid (BALF). AnxA1 mitigated the inflammatory response in the pulmonary tissue by lowering the levels of IL-1β, IL-6, and TNF-α in BALF of ALI mice. Additionally, AnxA1 attenuated oxidative stress in lung tissues of ALI mice by restoring the activity of catalase (CAT), SOD, and glutathione (GSH) but reducing the levels of malondialdehyde (MDA). We also found that AnxA1 suppressed activation of the NLRP3 signaling pathway. Mechanistically, AnxA1 activated the Nrf2/HO-1 signaling pathway while preventing the activation of NF-κB.
conclusionCollectively, these findings suggest that AnxA1 alleviates LPS-induced ALI and might be a promising novel therapeutic agent against LPS-induced ALI.
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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 Socratic graph.