RESUMO
Autophagy is a self-protect cellular mechanism by which the unneeded cellular structure or impaired protein are targeted to degeneration. Acute pancreatitis (AP) is associated with autophagy tightly. This article is aimed to mainly elaborate the phenomenon that AP can be triggered by impaired autophagy and the mechanism of AP exacerbation by damaged autophagy. In AP, the reasons of impaired autophagy is dysfunction of cathepsins and lysosome associated membrane protein, which present as vacuoles accumulation in acinar cells and combination disorder of autophagolysosome, finally to activation of trypsin. By the relocation of high mobility group box 1 (HMGB1) and promotion of mitochondrial permeability transition (MPT), impaired autophagy aggravates AP. Understanding the above mechanism has certain significance to the prevention and treatment of AP.
RESUMO
Autophagy is a self-protect cellular mechanism by which the unneeded cellular structure or impaired protein are targeted to degeneration. Acute pancreatitis (AP) is associated with autophagy tightly. This article is aimed to mainly elaborate the phenomenon that AP can be triggered by impaired autophagy and the mechanism of AP exacerbation by damaged autophagy. In AP, the reasons of impaired autophagy is dysfunction of cathepsins and lysosome associated membrane protein, which present as vacuoles accumulation in acinar cells and combination disorder of autophagolysosome, finally to activation of trypsin. By the relocation of high mobility group box 1 (HMGB1) and promotion of mitochondrial permeability transition (MPT), impaired autophagy aggravates AP. Understanding the above mechanism has certain significance to the prevention and treatment of AP.