Liao Yajin, Dong Yuan, Cheng Jinbo
The Brain Science Center, Beijing Institute of Basic Medical Sciences, No. 27 Taiping Road, Haidian District, Beijing 100039, China.
The State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Int J Mol Sci. 2017 Feb 10;18(2):248. doi: 10.3390/ijms18020248.
The mitochondrial calcium uniporter (MCU)-a calcium uniporter on the inner membrane of mitochondria-controls the mitochondrial calcium uptake in normal and abnormal situations. Mitochondrial calcium is essential for the production of adenosine triphosphate (ATP); however, excessive calcium will induce mitochondrial dysfunction. Calcium homeostasis disruption and mitochondrial dysfunction is observed in many neurodegenerative disorders. However, the role and regulatory mechanism of the MCU in the development of these diseases are obscure. In this review, we summarize the role of the MCU in controlling oxidative stress-elevated mitochondrial calcium and its function in neurodegenerative disorders. Inhibition of the MCU signaling pathway might be a new target for the treatment of neurodegenerative disorders.
线粒体钙单向转运体（MCU）——线粒体内膜上的一种钙单向转运体——在正常和异常情况下控制线粒体对钙的摄取。线粒体钙对于三磷酸腺苷（ATP）的产生至关重要；然而，过量的钙会诱导线粒体功能障碍。在许多神经退行性疾病中都观察到钙稳态破坏和线粒体功能障碍。然而，MCU在这些疾病发生发展中的作用和调控机制尚不清楚。在这篇综述中，我们总结了MCU在控制氧化应激升高时线粒体钙方面的作用及其在神经退行性疾病中的功能。抑制MCU信号通路可能是治疗神经退行性疾病的一个新靶点。
