Skip to main content
. 2022 Aug 12;12:927193. doi: 10.3389/fcimb.2022.927193

Figure 1.

Figure 1

HMGB1 could be released by acinar cells and other cells in both active and passive ways. It participates in the formation of NETs and induce other acinar cell necrosis to boost the inflammation, therefore enhance the pathological process of AP. Meanwhile, HMGB1 is involved in lung and intestinal injury secondary to AP and serves as a pain mediator.