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乙型肝炎病毒诱导肝损伤的潜在机制。

Potential mechanisms of hepatitis B virus induced liver injury.

作者信息

Suhail Mohd, Abdel-Hafiz Hany, Ali Ashraf, Fatima Kaneez, Damanhouri Ghazi A, Azhar Esam, Chaudhary Adeel Ga, Qadri Ishtiaq

机构信息

Mohd Suhail, Ashraf Ali, Ghazi A Damanhouri, Adeel GA Chaudhary, Ishtiaq Qadri, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah 21589, Saudi Arabia.

出版信息

World J Gastroenterol. 2014 Sep 21;20(35):12462-72. doi: 10.3748/wjg.v20.i35.12462.

DOI:10.3748/wjg.v20.i35.12462
PMID:25253946
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4168079/
Abstract

Chronic active hepatitis (CAH) is acknowledged as an imperative risk factor for the development of liver injury and hepatocellular carcinoma. The histological end points of CAH are chronic inflammation, fibrosis and cirrhosis which are coupled with increased DNA synthesis in cirrhotic vs healthy normal livers. The potential mechanism involved in CAH includes a combination of processes leading to liver cell necrosis, inflammation and cytokine production and liver scaring (fibrosis). The severity of liver damage is regulated by Hepatitis B virus genotypes and viral components. The viral and cellular factors that contribute to liver injury are discussed in this article. Liver injury caused by the viral infection affects many cellular processes such as cell signaling, apoptosis, transcription, DNA repair which in turn induce radical effects on cell survival, growth, transformation and maintenance. The consequence of such perturbations is resulted in the alteration of bile secretion, gluconeogenesis, glycolysis, detoxification and metabolism of carbohydrates, proteins, fat and balance of nutrients. The identification and elucidation of the molecular pathways perturbed by the viral proteins are important in order to design effective strategy to minimize and/or restore the hepatocytes injury.

摘要

慢性活动性肝炎(CAH)被认为是肝损伤和肝细胞癌发生的一个重要危险因素。CAH的组织学终点是慢性炎症、纤维化和肝硬化,这些与肝硬化肝脏相对于健康正常肝脏中DNA合成增加相关。CAH涉及的潜在机制包括导致肝细胞坏死、炎症和细胞因子产生以及肝脏瘢痕形成(纤维化)的多种过程的组合。肝损伤的严重程度由乙型肝炎病毒基因型和病毒成分调节。本文讨论了导致肝损伤的病毒和细胞因素。病毒感染引起的肝损伤影响许多细胞过程,如细胞信号传导、细胞凋亡、转录、DNA修复,进而对细胞存活、生长、转化和维持产生根本性影响。这种干扰的后果导致胆汁分泌、糖异生、糖酵解、解毒以及碳水化合物、蛋白质、脂肪的代谢和营养平衡的改变。识别和阐明被病毒蛋白干扰的分子途径对于设计有效的策略以最小化和/或恢复肝细胞损伤很重要。

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本文引用的文献

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Decreased expression of toll like receptor signaling molecules in chronic HBV infected patients.慢性乙肝感染患者中Toll样受体信号分子表达降低。
Hum Immunol. 2014 Jan;75(1):15-9. doi: 10.1016/j.humimm.2013.09.015. Epub 2013 Oct 9.
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Chronic hepatitis B infection.慢性乙型肝炎感染。
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Dual behavior of HCV Core gene in regulation of apoptosis is important in progression of HCC.HCV 核心基因在调控细胞凋亡方面的双重作用在 HCC 的进展中很重要。
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HBV genotypes: relevance to natural history, pathogenesis and treatment of chronic hepatitis B.乙肝病毒基因型:与慢性乙型肝炎自然史、发病机制及治疗的相关性
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Is there any value to hepatitis B virus genotype analysis?乙型肝炎病毒基因型分析有什么价值吗?
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The hepatitis B virus X protein elevates cytosolic calcium signals by modulating mitochondrial calcium uptake.乙型肝炎病毒 X 蛋白通过调节线粒体钙摄取来升高细胞浆钙信号。
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