Effect of IGF-1 on the balance between autophagy of dysfunctional mitochondria and apoptosis
Effect of IGF-1 on the balance between autophagy of dysfunctional mitochondria and apoptosis
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DOI：
10.1016/j.febslet.2004.10.040
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发表时间：
2004-11-19
期刊：
影响因子：
3.5
通讯作者：
Cohen, A
中科院分区：
文献类型：
--
作者：
Gu, YP;Wang, CJ;Cohen, A
线粒体DNA（mtDNA）突变导致线粒体活性氧（ROS）的过度产生，缩短动物寿命。我们研究了通过自噬去除具有有害mtDNA突变的线粒体的机制。在没有血清的情况下孵育原代细胞和细胞系促进线粒体的自噬，线粒体DNA突变是有害的，但不影响正常的线粒体。通过添加IGF-1防止血清撤回对功能障碍的线粒体的自噬的影响。作为消除具有有害突变的线粒体的结果，过度的ROS产生（功能障碍的线粒体的特征）大大减少。线粒体自噬与药物诱导的细胞凋亡有共同的机制，包括线粒体过渡孔形成和ROS产生增加。(C)2004年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
Mutations in mitochondrial DNA (mtDNA) cause excessive production of mitochondrial reactive oxygen species (ROS) and shorten animal life span. We examined the mechanisms responsible for removal of mitochondria with deleterious mtDNA mutations by autophagy. Incubation of primary cells and cell lines in the absence of serum promotes autophagy of mitochondria with deleterious mtDNA mutations but spares their normal counterparts. The effect of serum withdrawal on the autophagy of dysfunctional mitochondria is prevented by the addition of IGF-1. As a result of the elimination of mitochondria with deleterious mutations, excessive ROS production, characteristic of dysfunctional mitochondria, is greatly reduced. Mitochondrial autophagy shares a common mechanism with mitochondrial-induced cell apoptosis, including mitochondrial transition pore formation and increased ROS production. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.