The Pathogenesis of Pancreatitis and the Role of Autophagy

被引:3
|
作者
Tsomidis, Ioannis [1 ]
Voumvouraki, Argyro [2 ]
Kouroumalis, Elias [1 ]
机构
[1] Univ Crete, Med Sch, Lab Gastroenterol & Hepatol, Iraklion 71500, Greece
[2] AHEPA Univ Hosp, Dept Internal Med 1, Thessaloniki 54621, Greece
关键词
pancreatitis; autophagy; mitochondrial abnormalities; ER stress; innate immunity; macrophages; fibrosis; ENDOPLASMIC-RETICULUM STRESS; NF-KAPPA-B; CERULEIN-INDUCED PANCREATITIS; TISSUE GROWTH-FACTOR; ALCOHOLIC CHRONIC-PANCREATITIS; PERMEABILITY TRANSITION PORE; INTERACTING PROTEIN-1 RIP1; LACTATED RINGERS SOLUTION; STELLATE CELL ACTIVATION; GLYCATION END-PRODUCTS;
D O I
10.3390/gastroent15020022
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
The pathogenesis of acute and chronic pancreatitis has recently evolved as new findings demonstrate a complex mechanism operating through various pathways. In this review, the current evidence indicating that several mechanisms act in concert to induce and perpetuate pancreatitis were presented. As autophagy is now considered a fundamental mechanism in the pathophysiology of both acute and chronic pancreatitis, the fundamentals of the autophagy pathway were discussed to allow for a better understanding of the pathophysiological mechanisms of pancreatitis. The various aspects of pathogenesis, including trypsinogen activation, ER stress and mitochondrial dysfunction, the implications of inflammation, and macrophage involvement in innate immunity, as well as the significance of pancreatic stellate cells in the development of fibrosis, were also analyzed. Recent findings on exosomes and the miRNA regulatory role were also presented. Finally, the role of autophagy in the protection and aggravation of pancreatitis and possible therapeutic implications were reviewed.
引用
收藏
页码:303 / 341
页数:39
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