[HTML][HTML] Genetic risk in chronic pancreatitis: the trypsin-dependent pathway
E Hegyi, M Sahin-Tóth - Digestive diseases and sciences, 2017 - Springer
Digestive diseases and sciences, 2017•Springer
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.
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.
Abstract
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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