Figure 7.

The mechanism of CD163 and PC involved in the process of ferroptosis in the glomerulus of LN patients. CD163 mediated the macrophages taken in haptoglobin–hemoglobin complexes, which come from RBC lysis. However, excessive phagocytosis of haptoglobin–hemoglobin complexes may result in excessive accumulation of iron and an increased amount of unstable iron pools within macrophages, leading to oxidative stress and ferroptosis. In glomerular epithelial cells, decreased PC expression reduced the level of NADPH and GSH pools and elevated the ROS accumulation, which may contribute to the occurrence of ferroptosis. Targeting ferroptosis in CD163⁺ macrophages and PC⁺ epithelial cells may provide promising therapeutic approaches in LN. RBC, red blood cell; NADPH, nicotinamide adenine dinucleotide phosphate; GSH, glutathione; LN, lupus nephritis; PC, pyruvate carboxylase; ROS, reactive oxygen species.