hUCMSC-exosomes attenuate acute lung injury by inhibiting ferroptosis in pulmonary microvascular endothelial cells through ribosomal protein RPS11 upregulation - PubMed
2 hours ago
- #Ferroptosis
- #Acute Lung Injury
- #Mitochondrial Function
- hUCMSC-exosomes were delivered via nebulization to treat acute lung injury (ALI) in an LPS-induced model, reducing lung damage, inflammation, and ferroptosis.
- The exosomes were internalized by pulmonary microvascular endothelial cells (HPMECs), improving mitochondrial function by transferring mitochondrial components and promoting mitochondria-encoded protein translation.
- Proteomic analysis identified ribosomal protein RPS11 as significantly upregulated; knocking down RPS11 blocked the exosomes' ability to inhibit ferroptosis and restore mitochondrial function.
- The study demonstrates that hUCMSC-exosomes act through RPS11 upregulation to enhance mitochondrial translation, inhibit ferroptosis in endothelial cells, and alleviate ALI, offering a non-invasive, cell-free therapy.