Figure 6.

The schematic diagram of the mechanisms through which lipopolysaccharide (LPS)-induced dephosphorylation of AMP-activated protein kinase (AMPK) potentiates inflammatory injury. Autophagy plays crucial roles in the limitation of inflammation, which is a tightly organized process. ULK1 is a key factor promoting the initiation of autophagy, it could be phorphorylated and inhibited by mammalian target of rapamycin (mTOR), a primary negative regulator of autophagy. AMPK functions as a suppressor of mTOR, it suppressed the activation of mTOR via phosphorylating TSC2, an inhibitor of mTOR, and thus prevents the inhibitory phosphorylation of ULK1 and promotes the induction of autophagy. LPS exposure induces the dephosphorylation and suppression of AMPK, which might result in weakened inhibition of mTOR, increased inhibitory phosphorylation of ULK1, and repressed autophagy. Thus, LPS-induced dephosphorylation of AMPK and repression of autophagy might be a novel mechanism underlying the development of inflammatory injury.