Abstract:

Ferroptosis of renal tubular epithelial cells not only leads to epithelial cell loss, but also converts lipid peroxidation events into immune signals. Hyperglycemia, ischemia-reperfusion, infectious inflammation and sustained oxidative stress promote ferroptotic stress and the release of damage-associated molecular patterns, oxidized lipids and extracellular vesicles. These signals activate macrophages and dendritic cells, amplifying inflammation, maladaptive repair and chronic remodeling. This review synthesizes the pathological contexts, signal-release mechanisms, immune sensing and disease outcomes of tubular ferroptosis. We also evaluate the value of related interventions and biomarkers.

Key words:

renal tubule, ferroptosis, immune microenvironment, damage-associated molecular pattern, extracellular vesicle, acute kidney injury to chronic kidney disease transition