Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated primarily from endogenous biochemical reactions in mitochondria, endoplasmic reticulum (ER), and peroxisomes. Typically, ROS/RNS correlate with oxidative damage and cell death; however, free radicals are also crucial for normal cellular functions, including supporting neuronal homeostasis. ROS/RNS levels influence and are influenced by antioxidant systems, including the catabolic autophagy pathways. Autophagy is an intracellular lysosomal degradation process by which invasive, damaged, or redundant cytoplasmic components, including microorganisms and defunct organelles, are removed to maintain cellular homeostasis. This process is particularly important in neurons that are required to cope with prolonged and sustained operational stress. Consequently, autophagy is a primary line of protection against neurodegenerative diseases. Parkinson’s is caused by the loss of midbrain dopaminergic neurons (mDANs), resulting in progressive disruption of the nigrostriatal pathway, leading to motor, behavioural, and cognitive impairments. Mitochondrial dysfunction, with associated increases in oxidative stress, and declining proteostasis control, are key contributors during mDAN demise in Parkinson’s. In this review, we analyse the crosstalk between autophagy and redoxtasis, including the molecular mechanisms involved and the detrimental effect of an imbalance in the pathogenesis of Parkinson’s.

中文翻译：

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帕金森氏症中的自噬和氧化还原稳态：关键平衡法

活性氧（ROS）和活性氮（RNS）主要由线粒体，内质网（ER）和过氧化物酶体的内源性生化反应产生。通常，ROS / RNS与氧化损伤和细胞死亡相关。但是，自由基对于正常的细胞功能（包括支持神经稳态）也至关重要。ROS / RNS水平影响抗氧化剂系统，包括分解代谢自噬途径，并受其影响。自噬是一种细胞内溶酶体降解过程，通过该过程可以去除侵入性，受损或多余的胞质成分（包括微生物和已消失的细胞器），以维持细胞体内稳态。对于需要长期和持续的操作压力的神经元，此过程尤为重要。所以，自噬是保护神经退行性疾病的主要方法。帕金森氏症是由中脑多巴胺能神经元（mDAN）的丧失引起的，导致黑纹状体途径的进行性破坏，从而导致运动，行为和认知障碍。帕金森氏病mDAN死亡期间，线粒体功能障碍以及氧化应激的增加和蛋白质稳态控制的下降是关键因素。在这篇综述中，我们分析了自噬和氧化还原之间的相互影响，包括所涉及的分子机制以及帕金森氏病发病机理中失衡的有害影响。导致运动，行为和认知障碍。帕金森氏病mDAN死亡期间，线粒体功能障碍以及氧化应激的增加和蛋白质稳态控制的下降是关键因素。在这篇综述中，我们分析了自噬和氧化还原之间的相互影响，包括所涉及的分子机制以及帕金森氏病发病机理中失衡的有害影响。导致运动，行为和认知障碍。帕金森氏病mDAN死亡期间，线粒体功能障碍以及氧化应激的增加和蛋白质稳态控制的下降是关键因素。在这篇综述中，我们分析了自噬和氧化还原之间的相互影响，包括所涉及的分子机制以及帕金森氏病发病机理中失衡的有害影响。