在老化的大脑中,不稳定的铁过载会重新编程微质和神经元来合成脂滴
Karina Cunha E Rocha1, Qian Xiang2, Chengjia Qian2
1Department of Medicine, Division of Endocrinology & Metabolism, University of California, San Diego; La Jolla, California, USA.
bioRxiv : the preprint server for biology
|November 24, 2025
概括
衰老的微质细胞和神经元由于线粒体-铁轴而积累脂质滴 (LDs). 这一由活性氧物种 (ROS) 驱动的过程破坏了细胞功能,并改变了神经元对铁的处理.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 衰老研究研究 衰老研究
背景情况:
- 脂质滴滴 (LD) 积累发生在老化中的小质细胞和神经元中.
- 这些非专业细胞中的LD与细胞功能障碍有关.
- LD形成的触发因素和细胞间影响尚未得到充分理解.
研究的目的:
- 为了识别老化微质中LD形成的上游驱动因素.
- 为了研究线粒体-铁轴在LD生物发生中的作用.
- 探索关于铁代谢的微质和神经元之间的细胞间通信.
主要方法:
- 研究了老化微质中的线粒体-铁轴.
- 评估了铁化和ROS清理对LD形成的影响.
- 分析了初级神经元上的铁应力微质中的条件介质.
- 检查了铁过载对神经元LD和相关途径的影响.
主要成果:
- 一个线粒体-铁轴通过ROS促进老化微质中的LD形成.
- 富含LD的微质体呈现出减少的线粒体质量,增加的可变铁,ROS和脂质过氧化.
- 铁压力小质细胞改变神经元的铁平衡,表明跨细胞合.
- 神经元中的铁过载会诱导LDs并激活协调的铁,ROS和脂质生成程序.
结论:
- 铁过载是微质和神经元中ROS依赖的LD生物发生的上游调节者.
- 微质神经轴在衰老过程中调节神经元的铁代谢.
- 针对线粒体-铁轴可能为与年龄相关的细胞功能障碍提供治疗策略.
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