An international team led by Nanyang Technological University and the University of Geneva reported that Enterococcus faecalis impairs chronic wound healing by generating reactive oxygen species through extracellular electron transport (EET), which activates the unfolded protein response in epithelial cells. Neutralizing EET restored cell migration and wound closure in preclinical models, the researchers reported in Science Advances. The study maps a direct mechanistic link between bacterial redox metabolism and host‑cell stress, offering a non‑antibiotic therapeutic angle to treat chronic wounds complicated by antibiotic‑resistant infections. Authors Guillaume Thibault and Kimberly Kline highlighted EET as a virulence mechanism that could be targeted to accelerate healing in diabetic foot ulcers and other chronic wounds. If translatable to humans, blocking bacterial EET or modulating host UPR could reduce amputations and treatment costs associated with infected chronic wounds.