The molecular mechanisms of acute kidney injury (AKI) remain unclear. Toll-like receptors
(TLRs), widely expressed on leukocytes and kidney epithelial cells, regulate innate and
adaptive immune responses. The present study examined the role of TLR signaling in
cisplatin-induced AKI. Cisplatin-treated wild-type mice had significantly more renal
dysfunction, histologic damage, and leukocytes infiltrating the kidney than similarly treated
mice with a targeted deletion of TLR4 [Tlr4 (−/−)]. Levels of cytokines in serum, kidney, and …