Further studies uncovered that treatment with BIBP 3226 blocked NPY-induced expression of Y1R at both mRNA and protein levels, thereby largely enhancing NF-κB-Mincle-Syk signaling and expression of IL-1β, TNFα, and IL-6 in the AKI kidney in a dose-dependent manner (Figure 7 and Supplementary Figure 6). Here, CLEC4E is linked to acute kidney injury.