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针对线粒体功能障碍和氧化应激以预防视网膜神经节细胞的神经退行性变

Targeting Mitochondrial Dysfunction and Oxidative Stress to Prevent the Neurodegeneration of Retinal Ganglion Cells.

作者信息

Catalani Elisabetta, Brunetti Kashi, Del Quondam Simona, Cervia Davide

机构信息

Department for Innovation in Biological, Agro-Food and Forest Systems (DIBAF), Università degli Studi della Tuscia, Largo dell'Università snc, 01100 Viterbo, Italy.

出版信息

Antioxidants (Basel). 2023 Nov 17;12(11):2011. doi: 10.3390/antiox12112011.

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

氧化还原稳态失衡会导致神经退行性变,包括与视觉系统相关的神经退行性变。线粒体对于提供能量至关重要,并负责多种细胞功能,是活性氧和/或氮物种的重要来源,反过来,它们又对自由基失衡敏感。功能失调的线粒体与视网膜病变的发生和发展有关,并直接参与视网膜神经元变性。视网膜神经节细胞(RGCs)是高能量消耗者,易受线粒体功能障碍影响,最终导致RGCs丢失。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,抗氧化治疗方法对神经元氧化损伤有效,是视网膜疾病面临的一个挑战。在此,我们强调了与RGCs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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/052b/10669517/c08d9448a516/antioxidants-12-02011-g001.jpg

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