Suen Der-Fen, Norris Kristi L, Youle Richard J
Biochemistry Section, Surgical Neurology Branch, NINDS, National Institutes of Health, Bethesda, MD 20892, USA.
Genes Dev. 2008 Jun 15;22(12):1577-90. doi: 10.1101/gad.1658508.
In healthy cells, mitochondria continually divide and fuse to form a dynamic interconnecting network. The molecular machinery that mediates this organelle fission and fusion is necessary to maintain mitochondrial integrity, perhaps by facilitating DNA or protein quality control. This network disintegrates during apoptosis at the time of cytochrome c release and prior to caspase activation, yielding more numerous and smaller mitochondria. Recent work shows that proteins involved in mitochondrial fission and fusion also actively participate in apoptosis induction. This review will cover the recent advances and presents competing models on how the mitochondrial fission and fusion machinery may intersect apoptosis pathways.
在健康细胞中，线粒体持续分裂并融合，形成一个动态的相互连接网络。介导这种细胞器分裂和融合的分子机制对于维持线粒体的完整性或许是必要的，可能是通过促进DNA或蛋白质质量控制来实现。在细胞凋亡过程中，当细胞色素c释放时以及半胱天冬酶激活之前，这个网络会瓦解，产生更多数量且更小的线粒体。最近的研究表明，参与线粒体分裂和融合的蛋白质也积极参与细胞凋亡的诱导过程。本综述将涵盖近期的进展，并呈现关于线粒体分裂和融合机制如何与细胞凋亡途径相互交叉的几种相互竞争的模型。
