由肠道微生物衍生的甲基胺加速宿主细胞衰老.
Hao Yang1, Tongyao Wang1, Chenglang Qian1
1National Clinical Research Center for Aging and Medicine, Huashan Hospital and MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Nature aging
|January 10, 2025
概括
肠道微生物随着衰老产生乙谷氨 (PAGln),加速细胞衰老. 针对这种途径可能会提供新的抗衰老疗法.
科学领域:
- 微生物学 微生物学
- 老年学是一门学科.
- 代谢学 代谢学 代谢学
背景情况:
- 肠道微生物群的组成和功能在衰老过程中显著影响宿主健康.
- 连接肠道微生物群与细胞衰老和衰老的机制尚未完全理解.
研究的目的:
- 研究肠道微生物群代谢物在驱动宿主细胞衰老中的作用.
- 阐明参与代谢物诱导衰老的分子途径.
主要方法:
- 对肠道微生物群和代谢产物的与年龄相关的变化进行分析 (乙酸[PAA]和乙胺[PAGln]).
- 使用细胞和小鼠模型进行体外和体内研究,以评估PAGln对衰老的影响.
- 研究信号通路,包括上腺体受体 (ADR) -AMP激活蛋白激酶 (AMPK),线粒体功能和DNA损伤.
主要成果:
- 老龄化改变了肠道微生物群,增加了PAA和PAGln的产生.
- 在细胞和小鼠模型中,PAGln会诱导衰老的表型.
- 通过ADR-AMPK信号传递,PAGln会触发线粒体功能障碍和DNA损伤.
结论:
- 肠道微生物群代谢物PAGln加速宿主细胞衰老.
- 阻止ADR信号传递或使用老化剂可以抑制PAGln诱导的衰老.
- PAGln代表了缓解与年龄相关的细胞衰退的潜在治疗标.
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