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丙型肝炎病毒感染:脂肪变性、胰岛素抵抗和氧化应激的分子途径。

Hepatitis C virus infection: molecular pathways to steatosis, insulin resistance and oxidative stress.

机构信息

Division of Clinical Pathology, University Hospitals, Geneva, Switzerland.

Division of Gastroenterology and Hepatology, University Hospitals, Geneva, Switzerland.

出版信息

Viruses. 2009 Sep;1(2):126-143. doi: 10.3390/v1020126. Epub 2009 Aug 11.

DOI:10.3390/v1020126
PMID:21994542
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3185489/
Abstract

The persistent infection with hepatitis C virus is a major cause of chronic liver disease worldwide. However, the morbidity associated with hepatitis C virus widely varies and depends on several host-related cofactors, such as age, gender, alcohol consumption, body weight, and co-infections. The objective of this review is to discuss three of these cofactors: steatosis, insulin resistance and oxidative stress. Although all may occur independently of HCV, a direct role of HCV infection in their pathogenesis has been reported. This review summarizes the current understanding and potential molecular pathways by which HCV contributes to their development.

摘要

丙型肝炎病毒的持续感染是全球慢性肝病的主要病因。然而,丙型肝炎病毒相关发病率差异很大,取决于多种宿主相关的合并因素,如年龄、性别、饮酒、体重和合并感染。本综述的目的是讨论其中三个合并因素:脂肪变性、胰岛素抵抗和氧化应激。尽管所有这些因素都可能独立于 HCV 发生,但已有报道称 HCV 感染在其发病机制中发挥直接作用。本综述总结了目前对 HCV 导致这些疾病发展的潜在分子途径的认识。

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本文引用的文献

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Treatment of insulin resistance with metformin in naïve genotype 1 chronic hepatitis C patients receiving peginterferon alfa-2a plus ribavirin.在初治的基因型1慢性丙型肝炎患者中,使用二甲双胍治疗胰岛素抵抗,这些患者同时接受聚乙二醇干扰素α-2a加利巴韦林治疗。
Hepatology. 2009 Dec;50(6):1702-8. doi: 10.1002/hep.23206.
2
Hepatitis C virus NS5A and core proteins induce oxidative stress-mediated calcium signalling alterations in hepatocytes.丙型肝炎病毒NS5A和核心蛋白诱导肝细胞中氧化应激介导的钙信号改变。
J Hepatol. 2009 May;50(5):872-82. doi: 10.1016/j.jhep.2008.12.026. Epub 2009 Feb 26.
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HCV induces oxidative and ER stress, and sensitizes infected cells to apoptosis in SCID/Alb-uPA mice.
From hepatitis A to E: A critical review of viral hepatitis.
从甲型肝炎到戊型肝炎:病毒性肝炎的批判性综述
World J Gastroenterol. 2021 Apr 28;27(16):1691-1715. doi: 10.3748/wjg.v27.i16.1691.
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Integrated stress response in hepatitis C promotes Nrf2-related chaperone-mediated autophagy: A novel mechanism for host-microbe survival and HCC development in liver cirrhosis.丙型肝炎的综合应激反应促进 Nrf2 相关伴侣介导的自噬:肝硬化中宿主-微生物生存和 HCC 发展的新机制。
Semin Cell Dev Biol. 2020 May;101:20-35. doi: 10.1016/j.semcdb.2019.07.015. Epub 2019 Aug 8.
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Counteraction of HCV-Induced Oxidative Stress Concurs to Establish Chronic Infection in Liver Cell Cultures.HCV 诱导的氧化应激拮抗作用有助于在肝细胞培养物中建立慢性感染。
Oxid Med Cell Longev. 2019 Feb 13;2019:6452390. doi: 10.1155/2019/6452390. eCollection 2019.
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The Multifaceted Roles of Autophagy in Flavivirus-Host Interactions.自噬在黄病毒-宿主相互作用中的多效性角色。
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Fatty acid synthase is up-regulated during hepatitis C virus infection and regulates hepatitis C virus entry and production.脂肪酸合酶在丙型肝炎病毒感染期间上调,并调节丙型肝炎病毒的进入和产生。
Hepatology. 2008 Nov;48(5):1396-403. doi: 10.1002/hep.22508.
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Insulin resistance is a major determinant of sustained virological response in genotype 1 chronic hepatitis C patients receiving peginterferon alpha-2b plus ribavirin.胰岛素抵抗是基因型 1 慢性丙型肝炎患者接受聚乙二醇干扰素α-2b 联合利巴韦林治疗后持续病毒学应答的主要决定因素。
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Pioglitazone in chronic hepatitis C not responding to pegylated interferon-alpha and ribavirin.吡格列酮用于对聚乙二醇化干扰素-α和利巴韦林无反应的慢性丙型肝炎患者。
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