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Review
. 2017 Sep;33(5):390-395.
doi: 10.1097/MOG.0000000000000380.

Genetic risk in chronic pancreatitis: the misfolding-dependent pathway

Miklós Sahin-Tóth  1
Affiliations
Review

Genetic risk in chronic pancreatitis: the misfolding-dependent pathway

Miklós Sahin-Tóth. Curr Opin Gastroenterol. 2017 Sep.

Abstract

Purpose of review: Genetic risk in chronic pancreatitis is partly due to mutations that cause misfolding of digestive enzymes and elicit endoplasmic reticulum stress. This review examines recent developments in this concept.

Recent findings: The best characterized misfolding variants in the highly expressed digestive proteases cationic trypsinogen (PRSS1) and carboxypeptidase A1 (CPA1) are strong, causative risk factors for chronic pancreatitis and may be associated with autosomal dominant hereditary pancreatitis.

Summary: Properties of misfolding digestive enzyme mutants indicate that endoplasmic reticulum stress is a highly relevant pathological mechanism and a potential therapeutic target in chronic pancreatitis.

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References

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    2. This is the most recent comprehensive review highlighting mechanisms of genetic risk in chronic pancreatitis associated with inappropriate trypsin activity.

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MeSH terms

Supplementary concepts