Additionally, research has shown that the expression of Lipocalin-2 (LCN2) increases significantly in sepsis-induced liver tissue of mice and lipopolysaccharide (LPS)-treated hepatocytes, mitigating oxidative stress-induced ferroptosis and reducing sepsis-induced liver injury [66], indicating the existence of the ferroptosis pathway in sepsis-induced liver injury. Here, LCN2 is linked to Sepsis.