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PGC1α驱动NAD生物合成,将氧化代谢与保护联系起来
Mei T Tran1,2, Zsuzsanna K Zsengeller1,2,3, Anders H Berg3,4
1Division of Nephrology and Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
Nature
|March 17, 2016
概括
通过控制尼古丁胺氨基二核酸 (NAD) 的产生,线粒体调节器PGC1α对于损伤后的恢复至关重要. 在缺乏PGC1α的小鼠中,补充尼胺 (NAM) 可以恢复NAD水平并改善功能.
科学领域:
- 肝脏病学
- 线粒体生物学
- 代谢调节
背景情况:
- 脏的高能量需求使其易受缺血损伤,导致急性损伤 (AKI).
- PGC1α是线粒体生物发生的关键调节剂,在细胞应激反应和代谢适应中起作用.
- NAD生物合成对于细胞能量代谢和修复过程至关重要.
研究的目的:
- 调查PGC1α在缺血损伤后的恢复中的作用.
- 确定NAD代谢与PGC1α介导的保护的关系.
- 在AKI中探索NAD前体的治疗潜力.
主要方法:
- 使用PGC1α缺乏 (Pgc1α-/-)) 和可诱导管状转基因 (iNephPGC1α) 的小鼠模型.
- 诱导缺血再输损伤以模拟AKI.
- 服用尼胺 (NAM) 补充剂,并评估NAD水平,脂质积累和功能.
- 研究了新的NAD合成途径和NAMPT,β-基酸和前列腺素PGE2的作用.
主要成果:
- Pgc1α-/ -小鼠表现出局部NAD缺乏,脂肪积累增加,脏在缺血后恢复受损.
- 外源性NAM补充剂使Pgc1α-/ -小鼠的NAD水平正常化,脂肪积累减少,功能改善.
- PGC1α对新兴的NAD合成酶进行上调,而其缺乏或AKI则减弱了这种途径.
- 通过β-基酸和前列腺素PGE2信号传导,NAM治疗逆转了已有的缺血性AKI,并预防了有毒的AKI.
结论:
- 通过调节NAD生物合成,PGC1α对于缺血损伤的恢复至关重要.
- 通过恢复NAD水平和激活保护途径,纳胺 (NAM) 补充剂代表了AKI的有希望的治疗策略.
- PGC1α-NAD-β-hydroxybutyrate-PGE2轴是预防缺血和毒性损伤的关键保护途径.
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