Fig. 6

Efficient encapsulation of let-7a-5p in MSCs-derived EVs via the CNP platform for acute lung injury treatment. Our results from the CNP platform, cell model, and rat model strongly confirm the following mechanism: The CNP platform provides an efficient method for producing engineered miRNA-enriched EVs with high specificity. These EV-let-7a-5p effectively attenuate Smad2/3 activation induced by TGF-β. Additionally, our observations indicate that EV-let-7a-5p regulate the induction of M2 macrophages in response to a fibrotic microenvironment resulting from pulmonary injury. Hence, EV-let-7a-5p hold promise for improving adverse lung conditions associated with ALI. The illustration was created with BioRender.com