ArticleInternational journal of nanomedicine2025
Apoptotic Vesicles Attenuate Acute Lung Injury
Article in International journal of nanomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Extracellular vesicles from mesenchymal stromal cells as a promising therapy for ARDS: a systematic review of preclinical studies.Frontiers in medicine · 2025Pooled it
- Review
- Apoptotic vesicles: from biological characteristics to clinical translational prospects.Journal of translational medicine · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- The Role of Traditional Chinese Medicine in Acute Lung Injury: Targeting Programmed Cell Death.Drug design, development and therapy · 2026Review
- Cell death in sepsis: unveiling new perspectives on organ dysfunction.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Acute respiratory distress syndrome (ARDS) is a life-threatening type of acute lung injury (ALI) characterized by elevated mortality rates and long-term effects. To date, no pharmacological treatment has proven effective for ARDS. Mesenchymal stem cell-derived apoptotic vesicles (apoVs) were recently found to have excellent therapeutic potential for inflammatory diseases. In this study, our aim was to investigate the therapeutic effects and underlying mechanisms of apoVs in ALI. Methods: ALI was induced in mice through intratracheal instillation of lipopolysaccharide (LPS). ApoVs were then administered two hours post-induction, and their impacts on platelet activation, neutrophil infiltration, and NETosis were assessed. Additionally, the role of CD73 in mediating these effects was thoroughly investigated. Results: ApoVs inhibit platelet activation, thereby impeding the infiltration of neutrophils into the lung and the initiation of NETosis, ultimately alleviating ALI. Remarkably, apoVs were enriched with CD73, which was critical for apoV-mediated repression of platelet activation and neutrophil NETosis, as well as the therapeutic effects observed in lung injury. Conclusion: This study reveals that apoVs inhibit platelet activity and neutrophil NETosis via CD73, offering an innovative and effective cell-free therapeutic strategy for ALI/ARDS.
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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.