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表皮NAD+枯竭驱动线粒体功能障碍,并导致肠道炎症

Elizabeth A Novak^1,2, Erin C Crawford³, Heather L Mentrup^1,2

¹Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.

Frontiers in immunology

|September 25, 2023

概括

在炎症性肠病 (IBD) 中降低的NAD+水平与PGC1α活性降低有关. 恢复NAD+水平可以改善结肠炎,但只有当PGC1α存在时,它才会改善结肠炎,这凸显了它在肠道健康中的关键作用.

科学领域:

线粒体生物学线粒体生物学
胃肠病学胃肠病学
分子医学是分子医学.

背景情况:

过氧酶增殖器激活的受体-联激活剂1-α (PGC1α) 的病理性下调有助于炎症性肠病 (IBD) 的病原发生.
在IBD中驱动PGC1α下调的确切机制尚不清楚.

研究的目的:

调查NAD+代谢在IBD期间PGC1α下调中的作用.
探索NAD+前体在实验性结肠炎中的治疗潜力.

主要方法:

在小鼠中诱导实验性结肠炎.
小鼠接受了尼古丁胺 рибоoside (NAD+前体) 的治疗.
测试包括西部污染,高分辨率呼吸计,NAD+量化和免疫沉.

主要成果:

在实验性大肠炎的小鼠和性大肠炎的人类的肠表皮中观察到显著的NAD+耗尽.
在实验性结肠炎中发现了增加的多ADP-ribose) 聚合酶-1 (PARP1) 活性,这是一个消耗NAD+的酶.
NAD+前体治疗减少了结肠炎的严重程度,恢复了线粒体功能,并增加了活性PGC1α水平.
治疗效果取决于PGC1α的存在,因为缺乏PGC1α的转基因小鼠没有显示任何益处.

结论:

PGC1α对于维护线粒体健康和肠表皮的恒常性至关重要.
通过PGC1α调节,NAD+代谢在IBD病原发生中发挥着关键作用.
像尼古丁胺核糖体这样的NAD+前体,代表了IBD的潜在治疗策略,取决于完整的PGC1α信号传递.

关键词:

在PGC1α中.大肠炎是一种大肠炎.尼古丁胺胺腺因二核酸是什么尼古丁胺胺里化物聚 (((ADP) рибоoside 聚合物的聚合物.

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