In CKD models, hypoxic renal tubular epithelial cells exhibit characteristics of ferroptosis, such as mitochondrial dysfunction, reduced GPX4, and increased 4-HNE, driving inflammation and fibrosis through the activation of the NLRP3 inflammasome in CD1+ DCs of the myeloid cell population, leading to elevated levels of IL-1β and IL-18 [119]. Here, GPX4 is linked to chronic kidney disease.