工程外泌体包裹miR-218-5p通过铁凋亡途径缓解PM2.5诱导的上皮间质转化的进展

核心信息

• 论文英文标题: Engineered exosomes encapsulated miR-218-5p alleviate the progression of PM2.5-induced epithelial-mesenchymal transition via ferroptosis pathway
• 期刊: Redox Biol
• 发表年份: 2026
• DOI: 10.1016/j.redox.2026.104290
• PMID/PMCID: 42419173; PMC13356701

研究概览

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.

核心发现

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 角色

雾化给药，引用ExoLoad负载kit和Exobrooch iRGD脂锚(靶向发生EMT的肺上皮细胞)，也采购了ContrExo 293F外泌体参考品CTE-06--文章没写

关联平台: Echosome®, EV Materials / Reference Materials, Research Reagents & Tools

关联服务与能力: Small RNA / Cargo Loading, Targeting Peptide / Surface Modification, EV Material / Reference Material Supply

关联产品或试剂: ExoLoad® Nucleic Acid Loading Kit, ExoBrooch™ Targeting Peptide/Lipid Anchor Kit, ContrExo® EV Reference Material

参考文献

原始论文: 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.