内皮NAD+-H2S信号网络的损伤是血管衰老的可逆原因
Abhirup Das1, George X Huang2, Michael S Bonkowski3
1Paul F. Glenn Center for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Laboratory for Ageing Research, Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, NSW 2052, Australia; Paul F. Glenn Center for Science of Aging Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Cell
|March 24, 2018
概括
尼古丁胺单核酸 (NMN) 通过激活SIRT1增加毛细血管密度,从而提高老鼠的血液流动和耐力. 运动和硫化进一步增强了这些抗衰老作用.
科学领域:
- 老龄化研究
- 血管生物学
- 代谢途径
背景情况:
- 毛细血管密度和血液流量随着年龄的增长而下降,导致死亡率和发病率.
- 包括尼古丁胺 mononucleotide (NMN) 在内的 NAD+ 前体可以通过激活 sirtuin deacylases (SIRT) 来逆转一些衰老方面.
- 内皮细胞中的Sirtuin 1 (SIRT1) 对于介导肌细胞的亲血管信号至关重要.
研究的目的:
- 研究SIRT1在与年龄相关的血液流量和毛细血管密度下降中的作用.
- 确定NMN补充剂在改善老年小鼠血管功能和耐力方面的有效性.
- 探索运动和硫化 (H2S) 与NMN的协同作用.
主要方法:
- 给老年小鼠使用NMN.
- 血液流动和毛细血管密度的评估.
- 对耐力性能进行评估.
- 研究SIRT1激活和H2S水平的作用.
主要成果:
- 在老年小鼠中,NMN治疗改善了血液流动和耐力.
- 这些改善与SIRT1依赖的毛细血管密度增加有关.
- 运动和增加的H2S水平增加了NMN的有益作用.
- H2S被确定为饮食限制模仿剂和内皮NAD+水平的调节剂.
结论:
- 通过NMN激活SIRT1可以抵消与年龄相关的血管功能下降.
- NMN 具有改善器官血液流动,提高人类表现和促进老年人的运动的潜力.
- 运动和H2S等联合干预措施可能进一步增强NAD+增强剂的抗衰老效果.
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