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Current Progress of Mitochondrial Quality Control Pathways Underlying the Pathogenesis of Parkinsons Disease

机译：帕金森氏病发病机制中线粒体质量控制途径的最新进展

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Parkinson's disease (PD), clinically characterized by motor and nonmotor symptoms, is a common progressive and multisystem neurodegenerative disorder, which is caused by both genetic and environmental risk factors. The main pathological features of PD are the loss of dopaminergic (DA) neurons and the accumulation of alpha-synuclein (α-syn) in the residual DA neurons in the substantia nigra pars compacta (SNpc). In recent years, substantial progress has been made in discovering the genetic factors of PD. In particular, a total of 19 PD-causing genes have been unraveled, among which some members have been regarded to be related to mitochondrial dysfunction. Mitochondria are key regulators of cellular metabolic activity and are critical for many important cellular processes including energy metabolism and even cell death. Their normal function is basically maintained by the mitochondrial quality control (MQC) mechanism. Accordingly, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a kind of neurotoxin, exerts its neurotoxic effects at least partially by producing its toxic metabolite, namely, 1-methyl-4-phenylpyridine (MPP+), which in turn causes mitochondrial dysfunction by inhibiting complex I and mimicking the key features of PD pathogenesis. This review focused on three main aspects of the MQC signaling pathways, that is, mitochondrial biogenesis, mitochondrial dynamics, and mitochondrial autophagy; hence, it demonstrates in detail how genetic and environmental factors result in PD pathogenesis by interfering with MQC pathways, thereby hopefully contributing to the discovery of novel potential therapeutic targets for PD.
机译：临床上以运动和非运动症状为特征的帕金森氏病（PD）是一种常见的进行性和多系统神经退行性疾病，由遗传和环境风险因素共同引起。 PD的主要病理特征是多巴胺能（DA）神经元的丢失和黑质致密部（SNpc）残留DA神经元中α-突触核蛋白（α-syn）的积累。近年来，在发现PD的遗传因素方面已取得实质性进展。特别是，已经揭示了总共19个引起PD的基因，其中一些成员被认为与线粒体功能障碍有关。线粒体是细胞代谢活性的关键调节剂，对于许多重要的细胞过程（包括能量代谢乃至细胞死亡）至关重要。它们的正常功能基本上由线粒体质量控制（MQC）机制维持。因此，一种神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）通过产生其有毒代谢产物1-甲基-4-苯基吡啶至少部分发挥其神经毒性作用。 （MPP +），进而通过抑制复合物I并模仿PD发病机理的关键特征而导致线粒体功能障碍。这篇综述集中在MQC信号通路的三个主要方面，即线粒体的生物发生，线粒体的动力学和线粒体的自噬。因此，它详细展示了遗传和环境因素如何通过干扰MQC途径导致PD发病，从而有望为发现PD的新型潜在治疗靶标做出贡献。

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