Genetic Risk in Chronic Pancreatitis: The Trypsin-Dependent Pathway

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...

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Detalles Bibliográficos
Autores principales: Hegyi, Eszter, Sahin-Tóth, Miklós
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2017
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5487703/
https://www.ncbi.nlm.nih.gov/pubmed/28536777
http://dx.doi.org/10.1007/s10620-017-4601-3
Descripción
Sumario: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.

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