• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

脓毒症中胆汁淤积的分子发病机制。

The molecular pathogenesis of cholestasis in sepsis.

作者信息

Bhogal Harjit K, Sanyal Arun J

机构信息

Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University School of Medicine, Richmond, VA 23298-0341, USA.

出版信息

Front Biosci (Elite Ed). 2013 Jan 1;5(1):87-96. doi: 10.2741/e598.

DOI:10.2741/e598
PMID:23276972
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4944118/
Abstract

Sepsis-induced cholestasis is a complication of infection. Infections cause systemic and intrahepatic increase in proinflammatory cytokines which result in impaired bile flow ie. cholestasis. Several other mediators of impairment in bile flow have been identified under conditions of sepsis such as increased nitric oxide production and decreased aquaporin channels. The development of cholestasis may also further worsen inflammation. The molecular basis of normal bile flow and mechanisms of impairment in sepsis are discussed.

摘要

脓毒症诱导的胆汁淤积是一种感染并发症。感染导致全身和肝内促炎细胞因子增加,从而导致胆汁流动受损,即胆汁淤积。在脓毒症情况下,还发现了其他几种导致胆汁流动受损的介质,如一氧化氮生成增加和水通道蛋白通道减少。胆汁淤积的发展也可能进一步加重炎症。本文讨论了正常胆汁流动的分子基础以及脓毒症中胆汁流动受损的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257b/4944118/b216e5924d55/nihms-789481-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257b/4944118/ff06f07401c2/nihms-789481-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257b/4944118/0525263c86ca/nihms-789481-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257b/4944118/b216e5924d55/nihms-789481-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257b/4944118/ff06f07401c2/nihms-789481-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257b/4944118/0525263c86ca/nihms-789481-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257b/4944118/b216e5924d55/nihms-789481-f0003.jpg

相似文献

1
The molecular pathogenesis of cholestasis in sepsis.脓毒症中胆汁淤积的分子发病机制。
Front Biosci (Elite Ed). 2013 Jan 1;5(1):87-96. doi: 10.2741/e598.
2
Mechanisms of disease: mechanisms and clinical implications of cholestasis in sepsis.疾病机制:脓毒症中胆汁淤积的机制及临床意义
Nat Clin Pract Gastroenterol Hepatol. 2006 Oct;3(10):574-85. doi: 10.1038/ncpgasthep0602.
3
LPS induces the TNF-alpha-mediated downregulation of rat liver aquaporin-8: role in sepsis-associated cholestasis.脂多糖诱导肿瘤坏死因子-α介导的大鼠肝脏水通道蛋白-8下调:在脓毒症相关性胆汁淤积中的作用
Am J Physiol Gastrointest Liver Physiol. 2008 Feb;294(2):G567-75. doi: 10.1152/ajpgi.00232.2007. Epub 2008 Jan 3.
4
[Sepsis associated cholestasis in adults].成人脓毒症相关性胆汁淤积
Harefuah. 2001 Jun;140(6):519-23, 565.
5
Sepsis and cholestasis.脓毒症和胆汁淤积症。
Clin Liver Dis. 2008 Feb;12(1):151-72, ix. doi: 10.1016/j.cld.2007.11.002.
6
The role of inflammation in cholestasis: clinical and basic aspects.炎症在胆汁淤积中的作用:临床和基础方面。
Semin Liver Dis. 2010 May;30(2):186-94. doi: 10.1055/s-0030-1253227. Epub 2010 Apr 26.
7
Pathophysiology of cholestasis.胆汁淤积的病理生理学
Hum Pathol. 1970 Mar;1(1):1-24. doi: 10.1016/s0046-8177(70)80002-8.
8
[Mechanisms of cytokine-induced cholestasis].[细胞因子诱导胆汁淤积的机制]
Rev Med Interne. 2000 May;21(5):467-9. doi: 10.1016/s0248-8663(00)88963-8.
9
Sepsis and cholestasis.脓毒症与胆汁淤积
Clin Liver Dis. 2004 Feb;8(1):83-94. doi: 10.1016/S1089-3261(03)00134-X.
10
Cholestatic liver (dys)function during sepsis and other critical illnesses.脓毒症和其他危重病期间的胆汁淤积性肝功能(障碍)。
Intensive Care Med. 2016 Jan;42(1):16-27. doi: 10.1007/s00134-015-4054-0. Epub 2015 Sep 21.

引用本文的文献

1
Dynamic nomogram predicts sepsis risk in patients with acute liver failure: Analysis of intensive care database with external validation.动态列线图预测急性肝衰竭患者的脓毒症风险:重症监护数据库分析及外部验证
World J Gastroenterol. 2025 Aug 21;31(31):105229. doi: 10.3748/wjg.v31.i31.105229.
2
Development of a nomogram to predict in-ICU mortality of elderly patients with sepsis-associated liver injury: an analysis of the MIMIC-IV database.用于预测脓毒症相关性肝损伤老年患者重症监护病房内死亡率的列线图的开发:MIMIC-IV数据库分析
Front Med (Lausanne). 2025 Mar 26;12:1516853. doi: 10.3389/fmed.2025.1516853. eCollection 2025.
3
Mechanisms of sepsis-induced acute liver injury: a comprehensive review.脓毒症诱导的急性肝损伤机制:综述
Front Cell Infect Microbiol. 2025 Feb 21;15:1504223. doi: 10.3389/fcimb.2025.1504223. eCollection 2025.
4
Acute-on-chronic liver failure (ACLF): the 'Kyoto Consensus'-steps from Asia.慢加急性肝衰竭(ACLF):来自亚洲的“京都共识”步骤
Hepatol Int. 2025 Feb;19(1):1-69. doi: 10.1007/s12072-024-10773-4. Epub 2025 Feb 17.
5
Multi-omic signatures of host response associated with presence, type, and outcome of enterococcal bacteremia.与肠球菌血症的存在、类型及转归相关的宿主反应的多组学特征。
mSystems. 2025 Feb 18;10(2):e0147124. doi: 10.1128/msystems.01471-24. Epub 2025 Jan 21.
6
Diagnosis and management of benign recurrent intrahepatic cholestasis and psychosocial stressors in an adolescent: A case report.青少年良性复发性肝内胆汁淤积症与心理社会应激源的诊断和管理:一例报告
World J Clin Cases. 2024 Jul 16;12(20):4427-4433. doi: 10.12998/wjcc.v12.i20.4427.
7
Bile acid metabolism and signaling in health and disease: molecular mechanisms and therapeutic targets.健康与疾病中的胆汁酸代谢及信号传导:分子机制与治疗靶点
Signal Transduct Target Ther. 2024 Apr 26;9(1):97. doi: 10.1038/s41392-024-01811-6.
8
Diagnostic and predictive ability of hyperbilirubinemia severity in cats: A multicenter retrospective study.猫高胆红素血症严重程度的诊断和预测能力:一项多中心回顾性研究。
J Vet Intern Med. 2024 Mar-Apr;38(2):1043-1050. doi: 10.1111/jvim.17005. Epub 2024 Feb 15.
9
The Hepatic Porphyrias: Revealing the Complexities of a Rare Disease.《肝性血卟啉病:揭示罕见病的复杂性》
Semin Liver Dis. 2023 Nov;43(4):446-459. doi: 10.1055/s-0043-1776760. Epub 2023 Nov 16.
10
Hepatobiliary long-term consequences of COVID-19: dramatically increased rate of secondary sclerosing cholangitis in critically ill COVID-19 patients.COVID-19 对肝胆系统的长期影响:危重症 COVID-19 患者继发硬化性胆管炎发生率显著增加。
Hepatol Int. 2023 Dec;17(6):1610-1625. doi: 10.1007/s12072-023-10521-0. Epub 2023 Apr 29.

本文引用的文献

1
Farnesoid X receptor activation inhibits inflammation and preserves the intestinal barrier in inflammatory bowel disease.法尼醇 X 受体激活可抑制炎症并维持炎症性肠病的肠道屏障。
Gut. 2011 Apr;60(4):463-72. doi: 10.1136/gut.2010.212159. Epub 2011 Jan 17.
2
The bile acid membrane receptor TGR5 as an emerging target in metabolism and inflammation.胆汁酸膜受体 TGR5 作为代谢和炎症的新兴靶点。
J Hepatol. 2011 Jun;54(6):1263-72. doi: 10.1016/j.jhep.2010.12.004. Epub 2010 Dec 9.
3
Systemic gut microbial modulation of bile acid metabolism in host tissue compartments.宿主组织腔隙中胆汁酸代谢的系统性肠道微生物调节。
Proc Natl Acad Sci U S A. 2011 Mar 15;108 Suppl 1(Suppl 1):4523-30. doi: 10.1073/pnas.1006734107. Epub 2010 Sep 13.
4
Bile acids as regulators of hepatic lipid and glucose metabolism.胆汁酸作为肝脏脂质和糖代谢的调节剂。
Dig Dis. 2010;28(1):220-4. doi: 10.1159/000282091. Epub 2010 May 7.
5
Nuclear receptors as drug targets in cholestasis and drug-induced hepatotoxicity.核受体作为胆汁淤积和药物性肝毒性的药物靶点。
Pharmacol Ther. 2010 Jun;126(3):228-43. doi: 10.1016/j.pharmthera.2010.03.005. Epub 2010 Apr 11.
6
Urinary metabolomics in Fxr-null mice reveals activated adaptive metabolic pathways upon bile acid challenge.在 Fxr 基因敲除小鼠的尿液代谢组学研究中发现,在胆汁酸刺激下激活了适应性代谢途径。
J Lipid Res. 2010 May;51(5):1063-74. doi: 10.1194/jlr.M002923. Epub 2009 Nov 9.
7
Altered expression of nuclear receptors affects the expression of metabolic enzymes and transporters in a rat model of cholestasis.核受体表达的改变影响胆汁淤积症大鼠模型中代谢酶和转运体的表达。
Biol Pharm Bull. 2009 Dec;32(12):2046-52. doi: 10.1248/bpb.32.2046.
8
The bile acid receptor FXR is a modulator of intestinal innate immunity.胆汁酸受体法尼醇X受体(FXR)是肠道固有免疫的调节因子。
J Immunol. 2009 Nov 15;183(10):6251-61. doi: 10.4049/jimmunol.0803978. Epub 2009 Oct 28.
9
High expression of the bile salt-homeostatic hormone fibroblast growth factor 19 in the liver of patients with extrahepatic cholestasis.胆汁盐稳态激素成纤维细胞生长因子19在肝外胆汁淤积患者肝脏中的高表达。
Hepatology. 2009 Apr;49(4):1228-35. doi: 10.1002/hep.22771.
10
Aquaporins: their role in cholestatic liver disease.水通道蛋白:它们在胆汁淤积性肝病中的作用。
World J Gastroenterol. 2008 Dec 14;14(46):7059-67. doi: 10.3748/wjg.14.7059.