ArticleBiomaterials research2025
Double-Responsive Macrophage-Derived Exosomes Alleviate Acute Lung Injury.
Article in Biomaterials research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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Who cites it
5 citing papers in PubMed.
- Review
- Low expression of miR-126 constitutes a risk factor for perioperative respiratory adverse events among pediatric patients under general anesthesia.BMC pediatrics · 2026Article
- Recent Advances in Exosome-Based Therapeutic Strategies for Acute Lung Injury: Mechanisms and Translational Advances.Antioxidants (Basel, Switzerland) · 2026Review
- Nano-Enabled Fluorescence Switching: A Novel Strategy for PDGFRβ Detection and TKI Therapy Monitoring.Research (Washington, D.C.) · 2026Article
- Natural products in treating sepsis-associated lung and liver injuries by mediating ferroptosis, current progress, and future perspective.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is one of the complications of sepsis, and macrophages play an important role in ALI. The aim of this research was to investigate the effects of epidermal growth factor receptor (EGFR) monoclonal antibody-modified chemokine (C-X-C motif) ligand 8 (CXCL8) overexpression of macrophage (CXCL8@M)-derived exosomes miR-126a-3p (EGFR@CXCL8@exo-miR-126a-3p) on sepsis ALI. CXCL8@M was obtained via macrophage infection of CXCL8 plasmid, and CXCL8-M-exo was obtained via an exosome extraction kit. In addition, hsa-miR-126-3p agomir [a specially chemically modified microRNA (miRNA) mimic, named miR-126-3p] was loaded in CXCL8@M-exo to form CXCR8@exo-miR-126a-3p via electroporation technology. Further, EGFR@CXCR8@exo-miR-126a-3p was obtained via EGFR monoclonal antibody-modified CXCR8@exo-miR-126a-3p. Lipopolysaccharide (LPS)-induced ALI models were used to evaluate the role and mechanism of EGFR@CXCR8@exo-miR-126a-3p on ALI. Single-cell sequencing and miRNA chip results showed that miR-126a-3p was mainly expressed in pulmonary macrophages and markedly decreased, while single-cell sequencing and immunofluorescence results showed that EGFR was expressed and significantly elevated in macrophages in ALI mice. miR-126a-3p and EGFR siRNA significantly inhibited polarization of M1 macrophage. The imaging results of small animals showed that EGFR@CXCL8-exo-miR-126a-3p has obvious macrophage targeting. The results showed that EGFR@CXCR8@exo-miR-126a-3p significantly inhibited M1 macrophage and increased Treg cells to exert anti-inflammatory effects. The mechanism of EGFR@CXCR8@exo-miR-126a-3p on ALI is mainly via inhibition of PIK3R2/NLRP3 signaling pathway and ferroptosis. This study provided a new treatment method for ALI.
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Registered trials
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