Sahin-Toth_2017_Curr.Opin.Gastroenterol_33_390

Reference

Title : Genetic risk in chronic pancreatitis: the misfolding-dependent pathway - Sahin-Toth_2017_Curr.Opin.Gastroenterol_33_390
Author(s) : Sahin-Toth M
Ref : Curr Opin Gastroenterol , 33 :390 , 2017
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.

PubMedSearch : Sahin-Toth_2017_Curr.Opin.Gastroenterol_33_390
PubMedID: 28650851

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Citations formats

Sahin-Toth M (2017)
Genetic risk in chronic pancreatitis: the misfolding-dependent pathway
Curr Opin Gastroenterol 33 :390

Sahin-Toth M (2017)
Curr Opin Gastroenterol 33 :390