PTGES2 and Sepsis: Further, at the cellular level, we overexpressed and knocked down mPGES-2 in renal tubular epithelial cells by transfection of mPGES-2 overexpression plasmids and siRNA, respectively, and utilized autophagy inhibitor and inducer to analyze whether mPGES-2 exerts its roles by regulating autophagy with the hope to reveal the roles of mPGES-2 in LPS-induced AKI and its underlying mechanisms and provide new ideas and experimental clues for the prevention and treatment of AKI caused by sepsis and other factors.