Department of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain; Multidisciplinary Institute for Environmental Studies "Ramon Margalef", University of Alicante, Alicante, Spain.
Department of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
Prog Retin Eye Res. 2014 Nov;43:17-75. doi: 10.1016/j.preteyeres.2014.07.001. Epub 2014 Jul 17.
Retinal neurodegenerative diseases like age-related macular degeneration, glaucoma, diabetic retinopathy and retinitis pigmentosa each have a different etiology and pathogenesis. However, at the cellular and molecular level, the response to retinal injury is similar in all of them, and results in morphological and functional impairment of retinal cells. This retinal degeneration may be triggered by gene defects, increased intraocular pressure, high levels of blood glucose, other types of stress or aging, but they all frequently induce a set of cell signals that lead to well-established and similar morphological and functional changes, including controlled cell death and retinal remodeling. Interestingly, an inflammatory response, oxidative stress and activation of apoptotic pathways are common features in all these diseases. Furthermore, it is important to note the relevant role of glial cells, including astrocytes, Müller cells and microglia, because their response to injury is decisive for maintaining the health of the retina or its degeneration. Several therapeutic approaches have been developed to preserve retinal function or restore eyesight in pathological conditions. In this context, neuroprotective compounds, gene therapy, cell transplantation or artificial devices should be applied at the appropriate stage of retinal degeneration to obtain successful results. This review provides an overview of the common and distinctive features of retinal neurodegenerative diseases, including the molecular, anatomical and functional changes caused by the cellular response to damage, in order to establish appropriate treatments for these pathologies.
视网膜神经退行性疾病,如年龄相关性黄斑变性、青光眼、糖尿病性视网膜病变和色素性视网膜炎,每种疾病都有不同的病因和发病机制。然而,在细胞和分子水平上,它们对视网膜损伤的反应是相似的,导致视网膜细胞的形态和功能损伤。这种视网膜变性可能由基因缺陷、眼内压升高、高血糖水平、其他类型的应激或衰老引发,但它们都经常引发一系列细胞信号,导致明确且相似的形态和功能变化,包括受控的细胞死亡和视网膜重塑。有趣的是,炎症反应、氧化应激和细胞凋亡途径的激活是所有这些疾病的共同特征。此外,需要注意胶质细胞(包括星形胶质细胞、 Müller 细胞和小胶质细胞)的相关作用,因为它们对损伤的反应对维持视网膜的健康或其变性至关重要。已经开发了几种治疗方法来保护视网膜功能或在病理条件下恢复视力。在这种情况下,应在视网膜变性的适当阶段应用神经保护化合物、基因治疗、细胞移植或人工装置,以获得成功的结果。本综述概述了视网膜神经退行性疾病的共同和独特特征,包括细胞对损伤的反应引起的分子、解剖和功能变化,以便为这些病变建立适当的治疗方法。