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首页> 美国卫生研究院文献>other >O-Linked β-N-acetylglucosamine (O-GlcNAc) Modification: A New Pathway to Decode Pathogenesis of Diabetic Retinopathy
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O-Linked β-N-acetylglucosamine (O-GlcNAc) Modification: A New Pathway to Decode Pathogenesis of Diabetic Retinopathy

机译：O链接的β-N-乙酰氨基葡萄糖（O-GlcNAc）修饰：解码糖尿病性视网膜病变发病机理的新途径。

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The incidence of diabetes continues to rise among all ages and ethnic groups worldwide. Diabetic retinopathy is a complication of diabetes that affects the retinal neurovasculature causing serious vision problems, including blindness. Its pathogenesis and severity is directly linked to the chronic exposure to high glucose conditions. No treatments are currently available to stop the development and progression of diabetic retinopathy. To develop new and effective therapeutic approaches, it is critical to better understand how hyperglycemia contributes to the pathogenesis of diabetic retinopathy at the cellular and molecular levels. We propose alterations in O-GlcNAc modification of target proteins during diabetes contribute to the development and progression of diabetic retinopathy. The O-GlcNAc modification is regulated through hexosamine biosynthetic pathway. We showed this pathway is differentially activated in various retinal vascular cells under high glucose conditions perhaps due to their selective metabolic activity. O-GlcNAc modification can alter protein stability, activity, interactions, and localization. By targeting the same amino acid residues (serine and threonine) as phosphorylation, O-GlcNAc modification can either compete or cooperate with phosphorylation. Here we will summarize the effects of hyperglycemia-induced O-GlcNAc modification on the retinal neurovasculature in a cell-specific manner, providing new insight into the role of O-GlcNAc modification in early loss of retinal pericytes and the pathogenesis of diabetic retinopathy.
机译：全世界所有年龄段和种族的糖尿病发病率都在继续上升。糖尿病性视网膜病是糖尿病的并发症，其影响视网膜神经脉管系统，引起严重的视力问题，包括失明。其发病机理和严重程度直接与长期暴露于高葡萄糖条件有关。目前尚无治疗方法可以阻止糖尿病性视网膜病的发生和发展。为了开发新的有效的治疗方法，至关重要的是更好地了解高血糖如何在细胞和分子水平上促进糖尿病性视网膜病的发病。我们提出在糖尿病期间靶蛋白的O-GlcNAc修饰的改变有助于糖尿病性视网膜病的发展和进展。 O-GlcNAc修饰通过己糖胺的生物合成途径来调节。我们显示了这种途径在高葡萄糖条件下的各种视网膜血管细胞中被差异激活，这可能是由于它们的选择性代谢活性所致。 O-GlcNAc修饰可以改变蛋白质的稳定性，活性，相互作用和定位。通过靶向与磷酸化相同的氨基酸残基（丝氨酸和苏氨酸），O-GlcNAc修饰可以竞争或协同磷酸化。在这里，我们将以细胞特异性方式总结高血糖诱导的O-GlcNAc修饰对视网膜神经脉管系统的影响，为O-GlcNAc修饰在视网膜周细胞的早期丢失和糖尿病性视网膜病变的发病机理中的作用提供新的见解。

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