Selenomethionine (Se-Met) in gelatin methacryloyl (GelMA) hydrogels modulates ferroptosis to attenuate skin aging. This study investigates the role of epidermal stem cells (EpiSCs) in skin aging and how Se-Met can counteract age-related changes. Transcriptomic and metabolomic analyses revealed that aging EpiSCs experience reduced expression of the Gpx gene family, particularly GPX4, and increased arachidonic acid (AA) metabolism, leading to enhanced ferroptosis. Se-Met, an antioxidant and UV-absorbing compound, can enhance GPX4 expression, thereby protecting EpiSCs from AA-induced mitochondrial damage and ferroptosis. Se-Met was covalently grafted to UV-responsive GelMA hydrogels via AC-PEG-NHS tethers, enabling sustained and controlled release. The Se-Met@GelMA hydrogel accelerated wound healing in chronological aging mice models by inhibiting lipid peroxidation and ferroptosis. In photoaging models, the hydrogel significantly reduced inflammatory responses, extracellular matrix remodeling, and ferroptosis in UV-exposed mice. The hydrogel also demonstrated photoprotective effects, reducing skin damage and TEWL. The Se-Met@GelMA hydrogel showed excellent mechanical properties, sustained drug release, and biocompatibility, making it a promising candidate for clinical applications in skin repair and regeneration.Selenomethionine (Se-Met) in gelatin methacryloyl (GelMA) hydrogels modulates ferroptosis to attenuate skin aging. This study investigates the role of epidermal stem cells (EpiSCs) in skin aging and how Se-Met can counteract age-related changes. Transcriptomic and metabolomic analyses revealed that aging EpiSCs experience reduced expression of the Gpx gene family, particularly GPX4, and increased arachidonic acid (AA) metabolism, leading to enhanced ferroptosis. Se-Met, an antioxidant and UV-absorbing compound, can enhance GPX4 expression, thereby protecting EpiSCs from AA-induced mitochondrial damage and ferroptosis. Se-Met was covalently grafted to UV-responsive GelMA hydrogels via AC-PEG-NHS tethers, enabling sustained and controlled release. The Se-Met@GelMA hydrogel accelerated wound healing in chronological aging mice models by inhibiting lipid peroxidation and ferroptosis. In photoaging models, the hydrogel significantly reduced inflammatory responses, extracellular matrix remodeling, and ferroptosis in UV-exposed mice. The hydrogel also demonstrated photoprotective effects, reducing skin damage and TEWL. The Se-Met@GelMA hydrogel showed excellent mechanical properties, sustained drug release, and biocompatibility, making it a promising candidate for clinical applications in skin repair and regeneration.