An international team led by Nanyang Technological University and the University of Geneva identified extracellular electron transport (EET) in Enterococcus faecalis as a mechanism that generates reactive oxygen species (ROS) and activates the unfolded protein response (UPR) in epithelial cells, impairing wound closure. The preclinical work—reported in Science Advances—showed EET‑driven ROS production blocked keratinocyte migration in mouse models and human cells, and that neutralizing this pathway restored healing. The study establishes a direct link between bacterial redox metabolism and host cell dysfunction, suggesting new therapeutic angles for chronic, infected wounds—especially those complicated by antibiotic‑resistant organisms. The authors propose targeting EET or downstream UPR activation as an adjunct to antimicrobial therapy to accelerate repair in diabetic foot ulcers and other chronic wounds.