病原体加速人类衰老的特征:对分子机制的审查
Amy D Proal1, Michael B VanElzakker2
1PolyBio Research Foundation, Medford, MA, USA; Cohen Center for Recovery from Complex Chronic Illness, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Ageing research reviews
|August 9, 2025
概括
持续性感染,包括病毒和细菌病原体,通过破坏细胞过程和免疫信号,加速人类的衰老. 解决这些感染可能是改善健康的关键,并开发新的衰老疗法.
科学领域:
- 老年学是一门学科.
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 老龄化模型往往忽略了慢性感染的影响.
- 人类一生都携带着持久性病原体 (病毒,细菌,寄生虫).
- 这些病原体可以影响宿主细胞和免疫反应.
研究的目的:
- 审查传染病原体加速衰老的机制.
- 探索病原体对与年龄有关的疾病的贡献.
- 讨论健康跨度干预如何针对感染.
主要方法:
- 在衰老中病原体与宿主相互作用的文献综述.
- 分析感染诱导衰老的分子机制.
- 讨论诊断和治疗策略.
主要成果:
- 病原体干扰宿主免疫力,线粒体,基因表达和表观遗传学.
- 感染可以劫持宿主线粒体并破坏长寿途径.
- 病原体活动有助于与年龄相关的疾病,如阿尔茨海默氏症.
- 许多病原体破坏了关键的免疫代谢信号通路 (mTOR,AMPK) 的调节.
结论:
- 持续性感染是衰老和与年龄有关的疾病的重要驱动因素.
- 健康跨度干预措施可能部分通过控制慢性感染而起作用.
- 需要改进的诊断来检测组织寄存的病原体.
- 将感染纳入衰老研究对于准确的模型和疗法至关重要.
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