Yuan Yang, Zhang Xiangnan, Zheng Yanrong, Chen Zhong
Department of Pharmacology, Key Laboratory of Medical Neurobiology (Ministry of Health of China), College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.
Neurosci Bull. 2015 Aug;31(4):395-406. doi: 10.1007/s12264-015-1544-6. Epub 2015 Jul 28.
The selective degradation of damaged or excessive mitochondria by autophagy is termed mitophagy. Mitophagy is crucial for mitochondrial quality control and has been implicated in several neurodegenerative disorders as well as in ischemic brain injury. Emerging evidence suggested that the role of mitophagy in cerebral ischemia may depend on different pathological processes. In particular, a neuroprotective role of mitophagy has been proposed, and the regulation of mitophagy seems to be important in cell survival. For these reasons, extensive investigations aimed to profile the mitophagy process and its underlying molecular mechanisms have been executed in recent years. In this review, we summarize the current knowledge regarding the mitophagy process and its role in cerebral ischemia, and focus on the pathological events and molecules that regulate mitophagy in ischemic brain injury.
自噬对受损或过多线粒体的选择性降解被称为线粒体自噬。线粒体自噬对于线粒体质量控制至关重要，并且与多种神经退行性疾病以及缺血性脑损伤有关。新出现的证据表明，线粒体自噬在脑缺血中的作用可能取决于不同的病理过程。特别是，有人提出线粒体自噬具有神经保护作用，并且线粒体自噬的调节在细胞存活中似乎很重要。由于这些原因，近年来已经进行了广泛的研究，旨在描绘线粒体自噬过程及其潜在的分子机制。在这篇综述中，我们总结了关于线粒体自噬过程及其在脑缺血中作用的当前知识，并重点关注调节缺血性脑损伤中线粒体自噬的病理事件和分子。
