由食驱动的氧化还原失衡促进了病毒诱导的铁化
Hui Jiang1, Yang Qu1, Xianjin Kan1
1Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai 200241, China.
Cell reports
|June 6, 2025
概括
病毒感染会触发过度反应性氧物种 (ROS),激活突变的氧-氧性质 (ATM) 诱导食 (氧体退化). 这个过程促进铁亡,一种编程细胞死亡的形式,将病毒感染与细胞死亡联系起来.
科学领域:
- 细胞生物学 细胞生物学
- 病毒学 病毒学
- 生物化学 生物化学
背景情况:
- 过氧体对于维持细胞的氧化还原平衡至关重要.
- 病毒感染往往会诱导氧化应激和过氧体退化,但机制尚不清楚.
- 了解病毒诱导的食症对于理解细胞对感染的反应至关重要.
研究的目的:
- 系统地研究病毒诱导的食在调节过氧体恒常的作用.
- 阐明将病毒感染,氧化应激和编程细胞死亡联系在一起的分子机制.
主要方法:
- 使用了纽卡斯尔病病毒 (NDV) 作为模型病原体.
- 研究了阿塔克西亚-泰朗基切塔西亚突变 (ATM) 激酶的激活和局部化.
- 分析了过氧体受体PEX5和自受体p62.2之间的相互作用.
- 评估反应性氧物种 (ROS) 和铁含量.
主要成果:
- NDV感染诱导了过度的ROS产量,激活了ATM.
- 激活的ATM促进了PEX5-p62相互作用,导致了pexophagy.
- 佩克索法基导致铁和ROS的积累,导致铁亡.
- 与囊泡性口炎病毒和H9N2禽流感病毒观察到类似的机制.
结论:
- 病毒诱导的食破坏了细胞的氧化还原恒温.
- 这种干扰促进铁亡,这是病毒感染的关键结果.
- 这项研究揭示了病毒发病,过氧体退化和编程细胞死亡之间的重要联系.
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