PDF(Pubmed)
Abstract：
The imbalance of redox homeostasis contributes to neurodegeneration, including that related to the visual system. Mitochondria, essential in providing energy and responsible for several cell functions, are a significant source of reactive oxygen and/or nitrogen species, and they are, in turn, sensitive to free radical imbalance. Dysfunctional mitochondria are implicated in the development and progression of retinal pathologies and are directly involved in retinal neuronal degeneration. Retinal ganglion cells (RGCs) are higher energy consumers susceptible to mitochondrial dysfunctions that ultimately cause RGC loss. Proper redox balance and mitochondrial homeostasis are essential for maintaining healthy retinal conditions and inducing neuroprotection. In this respect, the antioxidant treatment approach is effective against neuronal oxidative damage and represents a challenge for retinal diseases. Here, we highlighted the latest findings about mitochondrial dysfunction in retinal pathologies linked to RGC degeneration and discussed redox-related strategies with potential neuroprotective properties.
摘要：
氧化还原稳态的失衡有助于神经变性，包括与视觉系统相关的。线粒体,在提供能量和负责多种细胞功能方面至关重要，是活性氧和/或氮物质的重要来源，他们是，反过来,对自由基失衡敏感。功能失调的线粒体与视网膜病变的发展和进展有关，并直接参与视网膜神经元变性。视网膜神经节细胞(RGC)是对最终导致RGC损失的线粒体功能障碍敏感的较高能量消费者。适当的氧化还原平衡和线粒体稳态对于维持健康的视网膜状况和诱导神经保护至关重要。在这方面,抗氧化剂治疗方法对神经元氧化损伤是有效的，对视网膜疾病是一个挑战。这里,我们强调了与RGC变性相关的视网膜病变中线粒体功能障碍的最新发现,并讨论了具有潜在神经保护特性的氧化还原相关策略.
