This study investigates the modulation of ferroptosis to mitigate skin aging using selenomethionine (Se-Met) in gelatin methacryloyl hydrogels. Through transcriptomics and metabolomics analysis, the study reveals age-dependent alterations in the Gpx gene family and arachidonic acid (AA) metabolic networks, leading to enhanced ferroptosis. Se-Met, which enhances GPX4 expression, helps EpiSCs counteract AA-induced mitochondrial damage and ferroptosis. Se-Met is covalently grafted onto UV-responsive GelMA hydrogels via AC-PEG-NHS tethers for sustained and controlled release. The Se-Met@GelMA hydrogel effectively accelerates wound healing in chronological aging mice by inhibiting lipid peroxidation and ferroptosis, and reduces inflammatory responses, extracellular matrix remodeling, and ferroptosis in photoaging mice. These findings highlight the potential clinical applications of Se-Met@GelMA hydrogels in treating skin aging and chronic wounds.This study investigates the modulation of ferroptosis to mitigate skin aging using selenomethionine (Se-Met) in gelatin methacryloyl hydrogels. Through transcriptomics and metabolomics analysis, the study reveals age-dependent alterations in the Gpx gene family and arachidonic acid (AA) metabolic networks, leading to enhanced ferroptosis. Se-Met, which enhances GPX4 expression, helps EpiSCs counteract AA-induced mitochondrial damage and ferroptosis. Se-Met is covalently grafted onto UV-responsive GelMA hydrogels via AC-PEG-NHS tethers for sustained and controlled release. The Se-Met@GelMA hydrogel effectively accelerates wound healing in chronological aging mice by inhibiting lipid peroxidation and ferroptosis, and reduces inflammatory responses, extracellular matrix remodeling, and ferroptosis in photoaging mice. These findings highlight the potential clinical applications of Se-Met@GelMA hydrogels in treating skin aging and chronic wounds.