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乙型肝炎病毒感染肝细胞的外基因组通过METTL3-介导的m6A修改P2RX7mRNA诱导肝纤维化

Caixia Li¹, Jiaxin Zeng², Yongbo Liu¹

¹Department of Clinical Laboratory, Hospital of NanHai Economic Development Zone, Foshan, Guangdong, China.

Journal of biochemical and molecular toxicology

|December 17, 2025

概括

乙型肝炎病毒 (HBV) 外基因组通过增加稳定P2RX7.7的METTL3来促进肝纤维化. 这个METTL3/P2RX7轴驱动肝星细胞激活和纤维化,提供潜在的治疗点.

科学领域:

肝病学肝病学是一种肝病学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

已知由乙型肝炎病毒 (HBV) 衍生的外体细胞 (HBV-Exo) 促进肝纤维化.
METTL3和P2RX7与肝纤维化有关,但它们在HBV外媒纤维化中的确切作用尚不清楚.

研究的目的:

研究HBV-Exo诱导肝纤维化的分子机制,重点关注METTL3和P2RX7.
阐明METTL3/P2RX7轴在HBV-Exo驱动的肝星细胞 (HSC) 激活和肝纤维化中的作用.

主要方法:

从HBV复制肝细胞 (HBV-THLE-2-Exo) 中分离外体,并用LX-2 HSC进行化.
评估HSC的生存能力,扩散,入侵,迁移和纤维化标志物.
机理学研究包括MeRIP,RIP,RNA下拉和mRNA稳定性测试.
在体内验证使用CCl4诱导的肝纤维化小鼠模型.

主要成果:

在LX-2 HSC中,HBV-Exo增加了METTL3水平,并促进了LX-2 HSC中的扩散,入侵,迁移和纤维化标志物.
外体体中METTL3的枯竭减弱了这些亲纤维细胞效应.
通过一种依赖IGF2BP1-m6A的机制,METTL3稳定了P2RX7,P2RX7过度表达逆转了METTL3耗尽效应.
在体内,HBV-Exo使肝纤维化恶化.

结论:

一个新的METTL3 / P2RX7信号轴调解HBV-Exo诱导的HSC激活和肝纤维化.
这种外体介导的调节途径突出显示了METTL3和P2RX7作为肝纤维化的潜在治疗标.

关键词:

在METTL3中,METTL3是METTL3的第一个类型.外基因组是外基因组的组成部分.肝脏的恒星细胞.乙型肝炎病毒的感染.肝脏纤维化肝脏纤维化

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