Molecular mechanisms of alcoholic pancreatitis
Molecular mechanisms of alcoholic pancreatitis
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DOI：
10.1159/000090170
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发表时间：
2005-01-01
影响因子：
2.3
通讯作者：
Wilson, JS
中科院分区：
文献类型：
--
作者：
Apte, MV;Pirola, RC;Wilson, JS
酒精性胰腺炎是酒精滥用的主要并发症。由于只有少数酗酒者会发生胰腺炎，因此人们对确定可能赋予个体对该疾病易感性的因素非常感兴趣。已经评估了许多可能性，包括饮食，饮酒模式和一系列遗传因素。然而，目前尚未明确确定易感因素。相比之下，在酒精对胰腺的持续影响方面取得了相当大的进展。近年来，酒精性胰腺损伤的分子机制越来越多地被定义为腺泡细胞本身是酒精相关损伤的主要部位。现已确定腺泡细胞能够代谢酒精，酒精和/或其代谢产物对腺泡细胞的直接毒性作用可能使腺体在适当触发因子存在下易发生自体消化损伤。最近的一个重要进展涉及胰腺星状细胞的特征，越来越多地涉及酒精性胰腺纤维化。在这里，目前的概念有关的机制/途径介导酒精诱导的胰腺损伤的概述。版权所有（C）2005 S. Karger AG，巴塞尔。
Alcoholic pancreatitis is a major complication of alcohol abuse. Since only a minority of alcoholics develop pancreatitis, there has been a keen interest in identifying the factors that may confer individual susceptibility to the disease. Numerous possibilities have been evaluated including diet, drinking patterns and a range of inherited factors. However, at the present time, no susceptibility factor has been unequivocally identified. In contrast, considerable progress has been made with respect to the constant effects of alcohol on the pancreas. The molecular mechanisms of alcohol-induced pancreatic injury are being increasingly defined with an emphasis, in recent years, on the acinar cell itself as the principal site on ethanol-related damage. It has now been established that the acinar cell is capable of metabolizing alcohol and that the direct toxic effects of alcohol and/or its metabolites on acinar cells may predispose the gland to autodigestive injury in the presence of an appropriate triggering factor. A significant recent development relates to the characterization of pancreatic stellate cells, increasingly implicated in alcoholic pancreatic fibrosis. Here the current concepts regarding the mechanisms/pathways mediating alcohol-induced pancreatic injury are outlined. Copyright (C) 2005 S. Karger AG, Basel.