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与PSTI/SPINK1表达相关的胰腺炎易感性。

Susceptibility to pancreatitis related to PSTI/SPINK1 expression.

作者信息

Liddle Rodger A

机构信息

Department of Medicine, Duke University Medical Center, Erwin Road, Durham, NC 27710, USA.

出版信息

Gastroenterol Clin North Am. 2004 Dec;33(4):807-16. doi: 10.1016/j.gtc.2004.07.013.

Abstract

This article summarized several observations on the role of pancreatic secretory trypsin inhibitor in the pancreas. Although it long has been suspected that endogenous pancreatic trypsin inhibitors protect against inadvertent activation of trypsinogen, this hypothesis has gained strength from recent biochemical investigations and genetic studies of populations suffering from chronic pancreatitis. There is now considerable evidence from clinical disease associations and burgeoning experimental models that some forms of pancreatitis may be the result of an imbalance between active pancreatic proteases and their inhibitors within the pancreas. Future studies should clarify the precise molecular interactions between enzymes and inhibitors and how these may be manipulated to prevent or treat pancreatitis.

摘要

本文总结了关于胰腺分泌型胰蛋白酶抑制剂在胰腺中作用的若干观察结果。尽管长期以来人们一直怀疑内源性胰腺胰蛋白酶抑制剂可防止胰蛋白酶原意外激活,但这一假说已从近期对慢性胰腺炎患者群体的生化研究和基因研究中得到了有力支持。目前,来自临床疾病关联和新兴实验模型的大量证据表明,某些形式的胰腺炎可能是胰腺中活性胰腺蛋白酶与其抑制剂之间失衡的结果。未来的研究应阐明酶与抑制剂之间精确的分子相互作用,以及如何通过调控这些相互作用来预防或治疗胰腺炎。

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