Figure 1.

The programmed death of macrophages, ECs, and TECs in sepsis-AKI. In sepsis, PAMPs and/or DAMPs that are released from damaged tissues activate and increase the pro-inflammatory phenotype (M1) forms of macrophages, leading to the release of pro-inflammatory cytokines which can cause damage to the kidney tissue of bystanders. PAMPs/DAMPs and etc present in the plasma can induce the dysfunction and cell death of vascular ECs. Abnormalities in the contraction and relaxation of local blood vessels, as well as the formation of microthrombus, result in the restriction of local blood supply and microcirculation disorders. Apoptosis and pyroptosis of ECs result in the increasing of vascular permeability. Thereafter, a large amount of fluid, endotoxin and inflammatory factors and cells permeated into the renal interstitium, further exacerbating local hypoxia. The infiltrating inflammatory cells and inflammatory factors, as well as the ROS, attacked TECs. Finally, TECs undergo apoptosis, pyroptosis and necroptosis, leading to AKI.