酒精摄入加重乙型肝炎病毒诱导肝细胞癌机制的研究进展

摘要/Abstract

摘要： 慢性乙型肝炎病毒(HBV)感染是我国肝细胞癌(HCC)最主要的致病因素,而酒精摄入是促进HBV感染进展为HCC的重要协同危险因素。HBV感染合并酒精暴露人群的HCC发病风险显著升高,且存在发病年龄提前、肿瘤恶性程度更高、临床预后更差等特征,二者存在明确的协同致癌效应,但其具体分子机制尚未完全阐明。近年来的研究表明,酒精及其代谢产物主要通过干扰HBV生命周期、诱导氧化应激与DNA损伤、调控宿主免疫微环境、促进肝纤维化进展以及介导异常表观遗传修饰等多种途径,协同增强HBV的致癌效应。本文结合国内外最新研究成果,系统综述了酒精摄入加重HBV诱导HCC的分子机制,旨在为临床防治提供理论依据。

关键词: 乙型肝炎病毒, 酒精摄入, 肝细胞癌, 协同致癌, 氧化应激, 免疫逃逸

周利, 杨松. 酒精摄入加重乙型肝炎病毒诱导肝细胞癌机制的研究进展[J]. 肝脏, 2026, 31(6): 774-778.

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