Editorial: Mechanisms and therapeutic strategies in cellular injury and repair

Editorial on the Research Topic Mechanisms and therapeutic strategies in cellular injury and repairCellular injury is a common response to heterogeneous insults, such as ischemiareperfusion, toxicants, metabolic byproducts, infection, and oncologic stress.However, this response often converges on a limited set of interconnected hubs: oxidative stress, mitochondrial dysfunction, disrupted Ca 2+ homeostasis, immune activation, and regulated cell death.The nine articles collected in this Research Topic cover topics ranging from heart and kidney function to cancer, reproductive toxicology, and physiological remodeling.Together, they illustrate how advances in mechanisms, biomarkers, and intervention design can be applied to shared molecular logic while still respecting tissue-specific contexts.A central theme across this Research Topic is the role of the oxidative stress-lipid peroxidation axis in driving ferroptotic vulnerability in renal epithelial injury.In an infection context, Lu et al. report that Pseudomonas aeruginosa promotes lipid peroxidation via a secreted 15-lipoxygenase and compromises epithelial antioxidant defense by reducing GPX4 through lysosomal chaperone-mediated autophagy, thereby triggering ferroptosis.Strikingly, macrophages counter this vulnerability: M1 macrophage-derived NO, generated by iNOS, remotely suppresses epithelial ferroptosis even when thiol-based antioxidant capacity is limited.Complementing the infection-driven pathway, Zhang et al. link the reactive dicarbonyl methylglyoxal (MG) to kidney injury, showing that MG increases ROS, depletes glutathione, elevates lipid peroxidation, and triggers ferroptosis in renal tubular epithelial cells.Together, these studies expand the range of upstream routes into ferroptosis, from microbial effectors to metabolic carbonyl stress, and highlight translational opportunities, including limiting lipid peroxidation, preserving GPX4 activity, and modulating immune-derived protective signals. Ischemia-reperfusion injury (IRI) adds another dimension by coupling metabolic stress to immune-mediated amplification. Through integrated bulk and single-cell transcriptomic analyses across multiple IRI organ datasets, Zheng et al. identify ANXA1 and ARG2 as early