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首页> 外文期刊>Journal of Ophthalmology >Regulation of Posttranscriptional Modification as a Possible Therapeutic Approach for Retinal Neuroprotection
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Regulation of Posttranscriptional Modification as a Possible Therapeutic Approach for Retinal Neuroprotection

机译：转录后修饰的调控作为视网膜神经保护的可能治疗方法

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Understanding pathogenesis at the molecular level is the first step toward developing new therapeutic approaches. Here, we review the molecular mechanisms of visual dysfunction in two common diseases, innate chorioretinal inflammation and diabetic retinopathy, and the role of the ubiquitin-proteasome system (UPS) in both processes. In innate chorioretinal inflammation, interleukin-6 family ligands induce STAT3 activation in photoreceptors, which causes UPS-mediated excessive degradation of the visual substance, rhodopsin. In diabetic retinopathy, angiotensin II type 1 receptor (AT1R) signaling activates ERK in the inner layers of the retina, causing UPS-mediated excessive degradation of the synaptic vesicle protein, synaptophysin. This latter effect may decrease synaptic activity, in turn adversely affecting neuronal survival. Both mechanisms involve increased UPS activity and the subsequent excessive degradation of a protein required for visual function. Finally, we review the therapeutic potential of regulating the UPS to protect tissue function, citing examples from clinical applications in other medical fields.
机译：从分子水平了解发病机理是开发新治疗方法的第一步。在这里，我们回顾了两种常见疾病（先天性脉络膜视网膜炎和糖尿病性视网膜病）的视觉功能障碍的分子机制，以及泛素-蛋白酶体系统（UPS）在这两个过程中的作用。在先天性脉络膜视网膜炎中，白介素6家族配体诱导感光器中的STAT3活化，从而引起UPS介导的视质视紫红质的过度降解。在糖尿病性视网膜病中，血管紧张素II 1型受体（AT1R）信号激活视网膜内层的ERK，从而引起UPS介导的突触小泡蛋白突触素的过度降解。后一种作用可能会降低突触活性，进而对神经元存活产生不利影响。两种机制都涉及增加的UPS活动和随后视觉功能所需蛋白质的过度降解。最后，我们以其他医学领域的临床应用为例，回顾了调节UPS保护组织功能的治疗潜力。

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