HMGB1 and acute kidney injury: To test if NF-κB signaling might be involved in the regulation of HMGB1-mediated renal protection from AKI, we stimulated isolated renal tubular epithelial cells with HMGB1 (0.1 μg/mL) and observed increased phosphorylation of NF-κB p-p65 (Figure 6A), which is a prerequisite for NF-κB release, nuclear translocation, and NF-κB–induced gene transcription.