STING contributes to lipopolysaccharide-induced tubular cell inflammation and pyroptosis by activating endoplasmic reticulum stress in acute kidney injury
As the leading cause of AKI in hospitalized and critically ill patients, sepsis is characterized by inappropriate immune responses, overwhelming inflammation and multiple organ dysfunction. Unfortunately, septic AKI currently lacks targeted drug treatments and is associated with a high mortality rate. Stimulator of interferon genes (STING) has emerged as a critical component of innate immune and inflammatory responses. However, the role of STING in the pathogenesis of septic AKI remains unclear. The endotoxin LPS is a potent trigger of host defense and the most common cause of sepsis. Here, we explored the role of STING in LPS-induced AKI. Tubule-specific STING knockout mice were generated, and RNAseq analysis using renal cortices from WT, STING-cKO, WT + LPS and STING-cKO + LPS mice was performed to gain insight into the necessity of STING in the tubular damage of LPS-induced AKI.