ArticleJournal of extracellular vesicles2024
Extracellular vesicles derived from M2-like macrophages alleviate acute lung injury in a miR-709-mediated manner.
Article in Journal of extracellular vesicles, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 39 citations in OpenAlex.
- Organization from cell to tissue derived delivery systems for immunotherapy.Materials today. Bio · 2026Article
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- Extracellular vesicles in senescence-associated chronic lung diseases.Chinese medical journal · 2026Review
- Pharmaceutical therapies for pyroptosis in lung injury.Inflammopharmacology · 2026Review
- Bone Marrow Stem Cell Exosomes Protect Lung Cells from Oxygen Damage by Regulating miR-23a-3p/Slc7a2 Pathway.The journal of gene medicine · 2026Article
- Review
- Engineered M2 macrophage-derived vesicles deliver DNase I for cfDNA clearance and multi-organ protection in sepsis.International journal of pharmaceutics: X · 2026Article
- Parabacteroides goldsteinii-derived outer membrane vesicles alleviate acute lung injury via modulation of bile acid metabolism.Journal of nanobiotechnology · 2026Article
- Hypoxia-preconditioned mesenchymal stromal cell-derived exosomes attenuate LPS-induced acute lung injury and early epithelial remodeling in mice: evidence for a miR-486a-5p-Skp2-GATA4 axis.Respiratory research · 2026Article
- Particle Phagocytosis Amplifies Secretion of Small Extracellular Vesicles in Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Low-concentration cholesterol modification enhancesRSC advances · 2026Article
- Functional remodeling of iNKT cells by sulfatide-reactive type II NKT cells reprograms alveolar macrophages to alleviate lung ischemia-reperfusion injury.Communications biology · 2026Article
- GPR43 alleviates LPS-induced acute lung injury by inhibiting NLRP3 inflammasome activation via β-arrestin 2.Biology direct · 2026Article
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Lipoxin A4 AttenuatesJournal of inflammation research · 2026Article
- Alveolar dysregulation of host response in pneumonia and ARDS: implications for immune modulation and infection.Annals of intensive care · 2026Review
- Unraveling the synergy of inflammation and apoptosis in sepsis-induced acute lung injury: Insights and therapeutic perspectives (Review).Molecular medicine reports · 2026Review
- Inhalable songorine-integrated lipid nanomedicine for targeted ARDS therapyActa pharmaceutica Sinica. B · 2026Article
- MiR-106a-5p in extracellular vesicles derived from alveolar epithelial cells mediates cognitive dysfunction induced by chronic intermittent hypoxia in mice through MAPK signaling pathway.Journal of neuroinflammation · 2025Article
- Organ-Specific Extracellular Vesicles in the Treatment of Ischemic Acute Organ Injury: Mechanisms, Successes, and Prospects.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is characterised by an uncontrolled inflammatory response, and current treatment strategies have limited efficacy. Although the protective effect of M2-like macrophages (M2φ) and their extracellular vesicles (EVs) has been well-documented in other inflammatory diseases, the role of M2φ-derived EVs (M2φ-EVs) in the pathogenesis of ALI/ARDS remains poorly understood. The present study utilised a mouse model of lipopolysaccharide-induced ALI to first demonstrate a decrease in endogenous M2-like alveolar macrophage-derived EVs. And then, intratracheal instillation of exogenous M2φ-EVs from the mouse alveolar macrophage cell line (MH-S) primarily led to a take up by alveolar macrophages, resulting in reduced lung inflammation and injury. Mechanistically, the M2φ-EVs effectively suppressed the pyroptosis of alveolar macrophages and inhibited the release of excessive cytokines such as IL-6, TNF-α and IL-1β both in vivo and in vitro, which were closely related to NF-κB/NLRP3 signalling pathway inhibition. Of note, the protective effect of M2φ-EVs was partly mediated by miR-709, as evidenced by the inhibition of miR-709 expression in M2φ-EVs mitigated their protective effect against lipopolysaccharide-induced ALI in mice. In addition, we found that the expression of miR-709 in EVs derived from bronchoalveolar lavage fluid was correlated negatively with disease severity in ARDS patients, indicating its potential as a marker for ARDS severity. Altogether, our study revealed that M2φ-EVs played a protective role in the pathogenesis of ALI/ARDS, partly mediated by miR-709, offering a potential strategy for assessing disease severity and treating 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 OpenQuestion graph.