Fig. 7From: Tofacitinib reduces acute lung injury and improves survival in a rat model of sepsis by inhibiting the JAK-STAT/NF-κB pathwayActivation of the JAK-STAT3 pathway. When inflammatory factors bind to receptors on the cell membrane, they induce receptors dimer formation and phosphorylation of JAK. Activated JAK can activate STAT3 in the cytoplasm to phosphorylate it, and the phosphorylated STAT3 binds to each other through the SH2 structural domain to form a dimer, which then enters the nucleus to bind to promoters to regulate gene expressionBack to article page