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Advances in the Pathogenesis of Pancreatitis

Zeyu Liu, Jie Li, Zhuohang Li, Yue Shi, Shengli Huang*

Abstract


One of the common acute abdominal diseases of acute pancreatitis, the global incidence of about 34~80 people per 100, 000 people
every year, in China and Europe and the United States have been increasing year by year[1]. The common causes of pancreatitis are biliary
diseases, alcohol, and hyperlipidemia. Other relatively rare etiologies include drugs, hypercalcemia, split pancreas division, infection, trauma,
genetic and autoimmune factors, and many more[2]. However, although the causes of diverse, but it has an important pathophysiological characteristics, namely from the clinical symptoms such as abdominal pain to progress to organ failure such as pancreatitis related lung injury
caused by acute respiratory distress syndrome, pancreatitis related renal injury caused by acute renal failure or pancreatic local complications
such as pancreatic pseudocyst and so on the pathophysiological process often need several days or even longer. Therefore, clarifying the core
molecular events involved in the occurrence and development of acute pancreatitis during this time period can greatly curb the development
of pancreatitis. Therefore, this paper will summarize the basic research progress of the pathogenesis of acute pancreatitis in recent years, in
order to have clinical guiding significance for the early treatment of acute pancreatitis.

Keywords


Acute pancreatitis; Pathogenesis; Pathological calcium signaling; Autophagy; Endoplasmic reticulum; Immune cells

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References


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