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急性实验性胰腺炎与核因子κB/Rel激活

Acute experimental pancreatitis and NF-kappaB/Rel activation.

作者信息

Algül Hana, Tando Yusuke, Schneider Günter, Weidenbach Hans, Adler Guido, Schmid Roland M

机构信息

Department of Internal Medicine I, University of Ulm, Germany.

出版信息

Pancreatology. 2002;2(6):503-9. doi: 10.1159/000066090.

Abstract

Acute pancreatitis is a serious disease with a high morbidity and an overall mortality rate of about 10%. However, in its most severe form, which is characterized by pancreatic necrosis, 20-30% of the patients die. Death is often the result of multiorgan dysfunction, including acute respiratory, kidney, and hepatic failure as well as generalized diffuse capillary leak water retention, hypoxia, and acid/base disturbance. The mechanisms by which distant organ systems are involved still remain obscure, but several lines of evidence suggest the participation of cytokines (IL-1, IL-6, and TNF-alpha) as a response to local tissue damage. A series of studies have now shed new light on the pivotal pathogenic role of the transcription factor NF-kappaB/Rel that binds to the promoter regions of many proinflammatory genes and regulates their transcription.

摘要

急性胰腺炎是一种严重疾病,发病率高,总体死亡率约为10%。然而,其最严重的形式是以胰腺坏死为特征,20%-30%的患者会死亡。死亡往往是多器官功能障碍的结果,包括急性呼吸、肾脏和肝功能衰竭以及全身性弥漫性毛细血管渗漏、水潴留、缺氧和酸碱紊乱。远处器官系统受累的机制仍不清楚,但有几条证据表明细胞因子(白细胞介素-1、白细胞介素-6和肿瘤坏死因子-α)参与其中,作为对局部组织损伤的一种反应。现在一系列研究为转录因子NF-κB/Rel的关键致病作用带来了新的认识,该转录因子与许多促炎基因的启动子区域结合并调节它们的转录。

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