The unfolded protein response signaling and retinal Müller cell metabolism.
The unfolded protein response signaling and retinal Müller cell metabolism.
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DOI：
10.4103/1673-5374.239431
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发表时间：
2018-11
影响因子：
6.1
通讯作者：
Zhang SX
中科院分区：
文献类型：
--
作者：
Kelly K;Wang JJ;Zhang SX
视网膜是身体中最需要能量的组织之一。与中枢神经系统中的大多数神经元一样，视网膜神经元消耗大量的三磷酸腺苷（ATP）来产生视觉信号并将信息传输到大脑。视网膜代谢的中断可引起神经元功能障碍和变性，从而导致严重的视力损害甚至失明。视网膜代谢的稳态受到多种信号通路的严格控制，例如未折叠蛋白反应（UPR），以及视网膜神经元和其他视网膜细胞类型（包括血管细胞和Müller胶质细胞）之间的密切相互作用。UPR是一种高度保守的适应性细胞反应，可以由许多生理应激源和病理生理条件触发。UPR的激活导致糖酵解速率、ATP产生、丝氨酸从头合成和己糖胺生物合成途径的变化，这些被认为是Müller神经胶质代谢的关键组成部分，并为周围神经元提供代谢支持。当这些通路被破坏时，神经变性迅速发生。本文就UPR在Müller胶质细胞中的研究进展作一综述，并着重介绍UPR通过调节Müller胶质细胞代谢在视网膜变性中的作用。
The retina is one of the most energy demanding tissues in the body. Like most neurons in the central nervous system, retinal neurons consume high amounts of adenosine-5′-triphosphate (ATP) to generate visual signal and transmit the information to the brain. Disruptions in retinal metabolism can cause neuronal dysfunction and degeneration resulting in severe visual impairment and even blindness. The homeostasis of retinal metabolism is tightly controlled by multiple signaling pathways, such as the unfolded protein response (UPR), and the close interactions between retinal neurons and other retinal cell types including vascular cells and Müller glia. The UPR is a highly conserved adaptive cellular response and can be triggered by many physiological stressors and pathophysiological conditions. Activation of the UPR leads to changes in glycolytic rate, ATP production, de novo serine synthesis, and the hexosamine biosynthetic pathway, which are considered critical components of Müller glia metabolism and provide metabolic support to surrounding neurons. When these pathways are disrupted, neurodegeneration occurs rapidly. In this review, we summarize recent advance in studies of the UPR in Müller glia and highlight the potential role of the UPR in retinal degeneration through regulation of Müller glia metabolism.
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