Moreover, following renal vascular endothelial injury, upregulated E-selectin, P-selectin, Intercellular adhesion molecule 1 (ICAM-1), and dipeptidase-1 (DPEP1) cooperate with corresponding integrins (including LFA-1 and Mac-1) to mediate neutrophil-endothelial adhesion post-AKI (24–27)。 Notably, the transient surge in plasma hepatocyte growth factor (HGF) after IRI activates the c-Met receptor on renal vascular endothelial cells, suppressing the NF-κB/ICAM-1 signaling pathway (28). Here, NFKB1 is linked to acute kidney injury.