Karidis Nikolaos P, Delladetsima Ioanna, Theocharis Stamatios
First Department of Pathology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Street, 11527 Athens, Greece.
Gastroenterol Res Pract. 2015;2015:654105. doi: 10.1155/2015/654105. Epub 2015 Mar 29.
Chronic hepatitis C virus (HCV) infection may eventually lead to progressive liver fibrosis and cirrhosis through a complex, multistep process involving hepatocyte death and regeneration. Despite common pathogenetic pathways present in all forms of liver cirrhosis irrespective of etiology, hepatocyte turnover and related molecular events in HCV-induced cirrhosis are increasingly being distinguished from even "similar" causes, such as hepatitis B virus- (HBV-) related cirrhosis. New insights in HCV-induced hepatocellular injury, differential gene expression, and regenerative pathways have recently revealed a different pattern of progression to irreversible parenchymal liver damage. A shift to the significant role of the host immune response rather than the direct effect of HCV on hepatocytes and the imbalance between antiapoptotic and proapoptotic signals have been investigated in several studies but need to be further elucidated. The present review aims to comprehensively summarize the current evidence on HCV-induced hepatocellular turnover with a view to outline the significant trends of ongoing research.
慢性丙型肝炎病毒（HCV）感染可能最终通过一个涉及肝细胞死亡和再生的复杂多步骤过程导致进行性肝纤维化和肝硬化。尽管所有形式的肝硬化，无论病因如何，都存在共同的发病机制，但丙型肝炎病毒诱导的肝硬化中的肝细胞更新及相关分子事件正越来越多地与其他“类似”病因区分开来，比如乙型肝炎病毒（HBV）相关肝硬化。最近，关于丙型肝炎病毒诱导的肝细胞损伤、差异基因表达和再生途径的新见解揭示了向不可逆实质性肝损伤进展的不同模式。宿主免疫反应而非丙型肝炎病毒对肝细胞的直接作用的重要作用转变以及抗凋亡和促凋亡信号之间的失衡已在多项研究中得到探讨，但仍需进一步阐明。本综述旨在全面总结目前关于丙型肝炎病毒诱导的肝细胞更新的证据，以期概述正在进行的研究的重要趋势。
