The preservation of mitochondrial function is of particular importance in neurons given the high energy requirements of action potential propagation and synaptic transmission. Indeed, disruptions in mitochondrial dynamics and quality control are linked to cellular pathology in neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. Here, we will discuss the role of ubiquitination by the E3 ligases: Parkin, MARCH5 and Mul1, and how they regulate mitochondrial homeostasis. Furthermore, given the role of Parkin and Mul1 in the formation of mitochondria-derived vesicles we give an overview of this area of mitochondrial homeostasis. We highlight how through the activity of these enzymes and MDV formation, multiple facets of mitochondrial biology can be regulated, ensuring the functionality of the mitochondrial network thus preserving neuronal health.

鉴于动作电位传播和突触传递的高能量需求，线粒体功能的保存在神经元中尤为重要。事实上，线粒体动力学和质量控制的中断与神经退行性疾病（如阿尔茨海默病和帕金森病）的细胞病理学有关。在这里，我们将讨论 E3 连接酶：Parkin、MARCH5 和 Mul1 泛素化的作用，以及它们如何调节线粒体稳态。此外，鉴于 Parkin 和 Mul1 在线粒体衍生囊泡形成中的作用，我们概述了线粒体稳态的这一领域。我们强调如何通过这些酶的活性和 MDV 的形成来调节线粒体生物学的多个方面，