Genetic Risk in Chronic Pancreatitis: The Trypsin-Dependent Pathway

被引：0
|
作者：
Eszter Hegyi
Miklós Sahin-Tóth
机构：
[1] Boston University Henry M. Goldman School of Dental Medicine,Center for Exocrine Disorders, Department of Molecular and Cell Biology
来源：
Digestive Diseases and Sciences | 2017年 / 62卷
关键词：
Pancreas; Pancreatitis; Digestive enzymes; Trypsinogen activation; Trypsin inhibitor; Chymotrypsin;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Genetic investigations have provided unique insight into the mechanism of chronic pancreatitis in humans and firmly established that uncontrolled trypsin activity is a central pathogenic factor. Mutations in the PRSS1, SPINK1, and CTRC genes promote increased activation of trypsinogen to trypsin by stimulation of autoactivation or by impairing protective trypsinogen degradation and/or trypsin inhibition. Here we review key genetic and biochemical features of the trypsin-dependent pathological pathway in chronic pancreatitis.
引用
收藏
页码：1692 / 1701
页数：9
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