Like in human HK-2 cells, in a rat model of septic AKI induced by CLP, circ-TLK1 was increased compared to the control rats; knockdown of circ-TLK1 in vivo reduced urinary levels of tubular injury markers such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), repressed oxidative stress markers such as ROS and proinflammatory cytokines such as IL-6 and IL-1β, and improved renal function with lower serum levels of creatinine and urea [37]. This evidence concerns the gene LCN2 and acute kidney injury.