Thornton Claire
Perinatal Brain Injury Group, Centre for the Developing Brain, Division of Imaging Sciences and Biomedical Engineering, King's College London, St. Thomas' Hospital, London SE1 7EH, U.K.
Neuronal Signal. 2017 Mar 24;1(2):NS20160020. doi: 10.1042/NS20160020. eCollection 2017 Apr.
Metabolically energetic organs, such as the brain, require a reliable source of ATP, the majority of which is provided by oxidative phosphorylation in the mitochondrial matrix. Maintaining mitochondrial integrity is therefore of paramount importance in highly specialized cells such as neurons. Beyond acting as cellular 'power stations' and initiators of apoptosis, neuronal mitochondria are highly mobile, transported to pre- and post-synaptic sites for rapid, localized ATP production, serve to buffer physiological and pathological calcium and contribute to dendritic arborization. Given such roles, it is perhaps unsurprising that recent studies implicate AMP-activated protein kinase (AMPK), a cellular energy-sensitive metabolic regulator, in triggering mitochondrial fission, potentially balancing mitochondrial dynamics, biogenesis and mitophagy.
代谢活跃的器官，如大脑，需要可靠的ATP来源，其中大部分由线粒体基质中的氧化磷酸化提供。因此，在神经元等高度特化的细胞中维持线粒体完整性至关重要。除了作为细胞的“发电站”和凋亡启动者外，神经元线粒体具有高度的移动性，被运输到突触前和突触后位点以进行快速的局部ATP生成，用于缓冲生理和病理状态下的钙，并有助于树突分支形成。鉴于这些作用，近期研究表明细胞能量敏感的代谢调节因子AMP激活的蛋白激酶（AMPK）参与触发线粒体裂变，可能平衡线粒体动力学、生物发生和线粒体自噬，这或许并不令人惊讶。
