Engineered exosomes encapsulated miR-218-5p alleviate the progression of PM2.5-induced epithelial-mesenchymal transition via ferroptosis pathway
Quick Facts
- Publication title: Engineered exosomes encapsulated miR-218-5p alleviate the progression of PM2.5-induced epithelial-mesenchymal transition via ferroptosis pathway
- Journal: Redox Biol
- Year: 2026
- DOI: 10.1016/j.redox.2026.104290
- PMID/PMCID: 42419173; PMC13356701
Research overview
Air pollution represents the greatest global environmental risk to human health, particularly regarding pulmonary fibrosis. Crucially, miR-218-5p was identified as a potential macrophage-derived exosomal miRNA targeting HO-1 to mediate ferroptosis-driven EMT in epithelial cells.
Key findings
Air pollution represents the greatest global environmental risk to human health, particularly regarding pulmonary fibrosis.
5) contributes most significantly to global mortality and disease burden.
5-induced pulmonary fibrosis, concomitant with iron deposition and disrupted lipid peroxide metabolism.
5-exposed macrophage induced ferroptosis, thereby driving EMT in epithelial cells.
Echo Biotech Role
Echo Biotech contributed cargo loading, targeting-peptide/surface modification, EV material/reference-material supply; the study also used or cited ExoLoad®, ExoBrooch™, ContrExo®.
Related platforms: Echosome®, EV Materials / Reference Materials, Research Reagents & Tools
Related services and capabilities: Small RNA / Cargo Loading, Targeting Peptide / Surface Modification, EV Material / Reference Material Supply
Related products or reagents: ExoLoad® Nucleic Acid Loading Kit, ExoBrooch™ Targeting Peptide/Lipid Anchor Kit, ContrExo® EV Reference Material
References
Original publication: Engineered exosomes encapsulated miR-218-5p alleviate the progression of PM2.5-induced epithelial-mesenchymal transition via ferroptosis pathway Redox biology. 2026. DOI: 10.1016/j.redox.2026.104290. PMID/PMCID: 42419173; PMC13356701.