Cerebral ischemia is a neurological disorder associated with complex pathological mechanisms, including autophagic degradation of neuronal mitochondria, or termed mitophagy, following ischemic events. Despite being well-documented, the cellular and molecular mechanisms underlying the regulation of neuronal mitophagy remain unknown. So far, the evidence suggests neuronal autophagy and mitophagy are separately regulated in ischemic neurons, the latter being more likely activated by reperfusional injury. Specifically, given the polarized morphology of neurons, mitophagy is regulated by different neuronal compartments, with axonal mitochondria being degraded by autophagy in the cell body following ischemia–reperfusion insult. A variety of molecules have been associated with neuronal adaptation to ischemia, including PTEN-induced kinase 1, Parkin, BCL2 and adenovirus E1B 19-kDa-interacting protein 3 (Bnip3), Bnip3-like (Bnip3l) and FUN14 domain-containing 1. Moreover, it is still controversial whether mitophagy protects against or instead aggravates ischemic brain injury. Here, we review recent studies on this topic and provide an updated overview of the role and regulation of mitophagy during ischemic events.

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靶向缺血性中风中的神经元线粒体自噬：更新

脑缺血是一种与复杂病理机制相关的神经系统疾病，包括缺血事件后神经元线粒体的自噬降解，或称为线粒体自噬。尽管有据可查，但调节神经元线粒体自噬的细胞和分子机制仍然未知。到目前为止，有证据表明神经元自噬和线粒体自噬在缺血神经元中分别受到调节，后者更可能被再灌注损伤激活。具体而言，鉴于神经元的极化形态，线粒体自噬受不同的神经元区室调节，轴突线粒体在缺血再灌注损伤后被细胞体中的自噬降解。多种分子与神经元对缺血的适应有关，包括 PTEN 诱导的激酶 1、Parkin、BCL2 和腺病毒 E1B 19-kDa 相互作用蛋白 3 (Bnip3)、Bnip3 样 (Bnip3l) 和包含 FUN14 结构域的 1。此外，线粒体自噬是预防还是加重缺血性脑损伤仍存在争议。在这里，我们回顾了最近关于该主题的研究，并提供了关于线粒体自噬在缺血事件中的作用和调节的最新概述。