Neurodegenerative diseases, a subset of age-driven diseases, have been known to exhibit increased oxidative stress. The resultant increase in reactive oxygen species (ROS) has long been viewed as a detrimental byproduct of many cellular processes. Despite this, therapeutic approaches using antioxidants were deemed unsuccessful in circumventing neurodegenerative diseases. In recent times, it is widely accepted that these toxic by-products could act as secondary messengers, such as hydrogen peroxide (H₂O₂), to drive important signaling pathways. Notably, mitochondria are considered one of the major producers of ROS, especially in the production of mitochondrial H₂O₂. As a secondary messenger, cellular H₂O₂ can initiate redox signaling through oxidative post-translational modifications (oxPTMs) on the thiol group of the amino acid cysteine. With the current consensus that cellular ROS could drive important biological signaling pathways through redox signaling, researchers have started to investigate the role of cellular ROS in the pathogenesis of neurodegenerative diseases. Moreover, mitochondrial dysfunction has been linked to various neurodegenerative diseases, and recent studies have started to focus on the implications of mitochondrial ROS from dysfunctional mitochondria on the dysregulation of redox signaling. Henceforth, in this review, we will focus our attention on the redox signaling of mitochondrial ROS, particularly on mitochondrial H₂O₂, and its potential implications with neurodegenerative diseases.

已知神经退行性疾病是年龄驱动疾病的一个子集，会表现出增加的氧化应激。长期以来，活性氧 (ROS) 的增加一直被视为许多细胞过程的有害副产品。尽管如此，使用抗氧化剂的治疗方法被认为无法成功规避神经退行性疾病。最近，人们普遍认为这些有毒副产物可以作为次级信使，例如过氧化氢 (H ₂ O ₂ )，以驱动重要的信号通路。值得注意的是，线粒体被认为是 ROS 的主要生产者之一，尤其是在线粒体 H ₂ O ₂的生产中。作为第二信使，细胞 H ₂ O₂可以通过氨基酸半胱氨酸的巯基上的氧化翻译后修饰 (oxPTM) 启动氧化还原信号。目前已达成共识，即细胞 ROS 可通过氧化还原信号驱动重要的生物信号通路，研究人员已开始研究细胞 ROS 在神经退行性疾病发病机制中的作用。此外，线粒体功能障碍与各种神经退行性疾病有关，最近的研究开始关注功能失调的线粒体产生的线粒体活性氧对氧化还原信号失调的影响。今后，在这篇综述中，我们将关注线粒体 ROS 的氧化还原信号，尤其是线粒体 H ₂ O ₂，及其对神经退行性疾病的潜在影响。