新兴的NAD合成增强了线粒体功能,改善了健康
Elena Katsyuba1, Adrienne Mottis1, Marika Zietak2,3
1Laboratory of Integrative and Systems Physiology, Interfaculty Institute of Bioengineering, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Nature
|October 26, 2018
概括
抑制ACMSD酶可以提高细胞NAD+水平,增强线粒体功能,并可能保护脏和肝脏. 这一发现为代谢和与年龄相关的疾病提供了新的治疗途径.
科学领域:
- 生物化学
- 代谢途径
- 线粒体生物学
背景情况:
- 尼古丁胺二核酸 (NAD+) 对细胞能量和寿命至关重要.
- SIRTUIN 是一种依赖NAD+的酶,与改善新陈代谢和寿命有关.
- 新兴NAD+合成途径的调节是细胞健康的关键.
研究的目的:
- 调查α-氨基-β-碳糖酸-ε-半甲基脱碳酶 (ACMSD) 在NAD+调节中的作用.
- 探索ACMSD抑制作为提高NAD+水平和素活性的一种策略.
- 评估ACMSD抑制剂在组织保护方面的治疗潜力.
主要方法:
- 在Caenorhabditis elegans和小鼠模型中进行基因操纵.
- 对ACMSD进行药理抑制.
- 测量细胞NAD+水平和Sirtuin 1活动.
- 评估线粒体功能.
主要成果:
- 通过一种保存机制,ACMSD被确定为细胞NAD+水平的关键调节者.
- 抑制ACMSD增加了新的NAD+合成和Sirtuin 1活性.
- 在ACMSD抑制后观察到线粒体功能增强.
- 两种强效和选择性的ACMSD抑制剂的特征.
结论:
- ACMSD是细胞NAD+水平,素活性和线粒体平衡的关键调节剂.
- 抑制ACMSD是一种增强NAD+代谢的有希望的治疗策略.
- 由于ACMSD表达受限,ACMSD抑制剂可能对和肝脏组织提供保护性益处.
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