Ulva -derived extracellular vesicles alleviate liver injury through a 7-hydroxycoumarin-associated EGFR–AKT regulatory axis

-induced injury models, UEVs reduced oxidative damage, improved biochemical indicators of liver function, and attenuated early fibrotic responses. To explore the potential mechanism, untargeted metabolomics was integrated with network pharmacology to prioritize candidate cargos and signaling pathways. 7-Hydroxycoumarin (7-HC) was identified as a candidate component potentially associated with EGFR-related signaling. In TGF-β1-activated hepatic stellate cells, 7-HC reduced fibrotic activation and AKT phosphorylation in a pattern similar to that observed with pharmacological EGFR inhibition. These findings provide a practical approach for linking vesicle composition with biological activity and suggest that UEVs may act, in part, through a 7-HC-associated, AKT-sensitive signaling mechanism related to EGFR-associated pathways.