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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


[1] LEEPJ, PAPACHRISTOUGI. New insights into acute pan-creatitis[J]. Nat Rev Gastroenterol Hepatol, 2019, 16(8):479-496.

[2] PANDOL SJ, SALUJA AK, IMRIE CW, et al. Acutepan-creatitis:bench to the bedside[J]. Gastroenterology, 2007, 132:1127-1151.

[3] RARATY M, WARD J, ERDEMLI G, et al. Calcium-depend-ent enzyme activation and vacuole formation in the apical gran-ular region

of pancreatic acinar cells [J]. ProcNatlAcadSciUSA, 2000, 97(24):13126-13131.

[4] MARENINOVA O A, HERMANN K, FRENCH S W, et al. Impaired autophagic flux mediates acinar cell vacuole formation and

trypsinogen activation in rodent models of acute pancreati-tis[J]. JClinInvest, 2009, 119(11):3340-3355.

[5] SHERWOOD M W, PRIOR I A, VORONINA S G, et al. Ac-tivation of trypsinogen in large endocytic vacuoles of pancreatic acinar

cells[J]. ProcNatlAcadSciUSA, 2007, 104(13):5674-5679.

[6] BICZO G, VEGH E T, SHALBUEVA N, et al. Mitochondrial dysfunction, through impaired autophagy, leads to endoplasmic reticulum

stress, deregulated lipid metabolism, and pancreatitis in animal models[J]. Gastroenterology, 2018, 154(3):689-703.

[7] BERNARDI P, RASOLA A, FORTE M, et al. The mitochon-drial permeability transition pore:channel formation byF-ATP synthase,

integration in signal transduction, and role in patho-physiology[J]. PhysiolRev, 2015, 95(4):1111-1155.

[8] MUKHERJEE R, MARENINOVA O A, ODINOKOVA I V, et al. Mechanism of mitochondrial permeability transition pore induction

and damage in the pancreas:inhibition prevents acute pancreatitis by protecting production of ATP [J]. Gut, 2016, 65(8):1333-1346.

[9] Li H, Wen W, Luo J. Targeting endoplasmic reticulum stress as an effective treatment for alcoholic pancrea-titis[J]. Biomedicines, 2022,

10(1):108.

[10] Lukas J, PospechJ, Oppermann C, et al. Role of endo-plasmic reticulum stress and protein misfolding in dis-orders of the liver and

pancreas[J]. AdvMedSci, 2019, 64(2):315-323.




DOI: http://dx.doi.org/10.18686/mhr.v2i2.4134

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