Embryos have a striking ability to heal wounds rapidly and without scarring. Embryonic wound repair is a conserved process, driven by polarization of cell-cell junctions and the actomyosin cytoskeleton in the cells around the wound. However, the upstream signals that trigger cell polarization around wounds are unknown. We used quantitative in vivo microscopy in Drosophila and zebrafish embryos to identify reactive oxygen species (ROS) as a critical signal that orchestrates cell polarity around wounds. ROS promote trafficking of adherens junctions and accumulation of actin and myosin at the wound edge and are necessary for wound closure. We show that, in Drosophila, ROS drive wound healing in part through an ortholog of Src kinase, Src42A, which we identify as a redox sensor that promotes polarization of junctions and the cytoskeleton around wounds. We propose that ROS are a reparative signal that drives rapid embryonic wound healing in vertebrate and invertebrate species.