NFE2L2 and Sepsis: S1R exhibits potential in clearing ROS,[59] reducing mitochondrial oxidative stress[60] and myocardial apoptosis,[61] thus alleviating sepsis-induced myocardial injury via the Nrf2/HO1 signaling pathway.[62] Moreover, elevated IL-16 expression observed in myocardial cells and serum of septic mice compared to non-septic mice can be modulated by anti-IL-16 neutralizing antibodies through the Nrf2 pathway, thereby reducing myocardial cell apoptosis, enhancing cardiac function, and lowering septic mortality rates.[63]