Fig. 2

AMPK is the important trigger for macrophage polarisation. On the one hand, LPSs promote M1 polarisation through the NF-κB pathway and the secretion of inflammatory factors such as IL-12, IL-6 and TNF-α. On the other hand, activation of AMPK inhibits the NF-κB pathway by upregulating the expression of SIRT1 and CREB, thereby inhibiting M1 polarisation. AMPKα-knockout macrophages display M1 hyperpolarisation. IL-4 promotes the polarisation of M2 macrophages by activating the downstream STAT6/PPARγ pathway and the secretion of the anti-inflammatory factors IL-10 and IL-1Ra. STAT6 is akey transcription factor involved in IL-4-mediated M2 polarisation. On the other hand, activation of AMPK promotes the upregulation of STAT6 and PPARγ, thereby affecting the polarisation of M2 macrophages. LPS lipopolysaccharide, TLR toll-like receptor, SIRT1 sirtuin 1, CREB cAMP-response element-binding protein, NF-κB nuclear factor κB, IL interleukin, IL-4R interleukin-4 receptor, PPAR peroxisome proliferator-activated receptor, STAT signal transducers and activators of transcription, TNF tumour necrosis factor