An NTU Singapore–University of Geneva team published in Science Advances that Enterococcus faecalis uses extracellular electron transport (EET) to generate reactive oxygen species, activate the unfolded protein response in epithelial cells, and impair wound closure. Neutralizing the bacterial redox mechanism restored cell migration in preclinical models. The study links bacterial metabolism directly to host tissue dysfunction and identifies EET as a virulence mechanism amenable to therapeutic targeting. Translational work will focus on small molecules or biologics that block EET or modulate host stress responses to accelerate healing in infected chronic wounds.