TLR4 and acute kidney injury: The administration of HMGB1 to WT mice also ameliorated IRI-induced AKI — as shown by reduced neutrophil recruitment into the kidney and reduced serum creatinine levels — which was abolished in TLR4/Ksp-Cre mice, indicating that the specific binding of HMGB1 to TLR4 on renal tubular epithelial cells is required for the protection from IRI-induced AKI in vivo (Figure 4, A and B).