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慢性丙型肝炎病毒感染中肝癌发生的分子机制。

Molecular mechanisms of hepatocarcinogenesis in chronic hepatitis C virus infection.

机构信息

Department of Gastroenterology, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa, Japan.

出版信息

J Gastroenterol Hepatol. 2011 Jun;26(6):960-4. doi: 10.1111/j.1440-1746.2011.06723.x.

Abstract

Hepatitis C virus (HCV) infection is a major cause of hepatocellular carcinoma (HCC) and chronic liver disease worldwide. Recent developments and advances in HCV replication systems in vitro and in vivo, transgenic animal models, and gene expression profiling approaches have provided novel insights into the mechanisms of HCV replication. They have also helped elucidate host cellular responses, including activated/inactivated signaling pathways, and the relationship between innate immune responses by HCV infection and host genetic traits. However, the mechanisms of hepatocyte malignant transformation induced by HCV infection are still largely unclear, most likely due to the heterogeneity of molecular paths leading to HCC development in each individual. In this review, we summarize recent advances in knowledge about the mechanisms of hepatocarcinogenesis induced by HCV infection.

摘要

丙型肝炎病毒(HCV)感染是全球范围内导致肝细胞癌(HCC)和慢性肝脏疾病的主要原因。近年来,HCV 在体外和体内复制系统、转基因动物模型和基因表达谱分析方法方面的发展和进展,为 HCV 复制的机制提供了新的见解。它们还帮助阐明了宿主细胞的反应,包括激活/失活的信号通路,以及 HCV 感染的先天免疫反应与宿主遗传特征之间的关系。然而,HCV 感染诱导肝细胞恶性转化的机制在很大程度上仍不清楚,这很可能是由于导致每个个体 HCC 发展的分子途径的异质性所致。在这篇综述中,我们总结了 HCV 感染诱导肝癌发生机制的最新研究进展。

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