| [ Summary ] |
In acute pancreatitis, the pancreatic pro‒enzymes, packaged into the zymogen granules of the acinar cells, become activated and cause autodigestion due to several factors. Based on the progress of recent studies, the pathogenesis of acute pancreatitis has changed to a new multifaceted paradigm from the older trypsin paradigm. The activation of trypsin in the acinar cells is one of the key mechanisms involved in acute pancreatitis along with nuclear factor kappa B activation, which is also an important mechanism. Autophagy is a crucial cellular regulator, and excessive intracellular Ca2+ is a key initiator of acute pancreatitis. Endoplasmic reticulum stress has also been recognized in acute pancreatitis. Interleukin‒6 mediates pancreatitis‒induced lung injury associated with severe acute pancreatitis. Damage‒associated molecular patterns play an important role in the pathogenesis of acute pancreatitis. These inflammatory factors may lead to a systemic inflammatory response in acute pancreatitis. |