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糖基化蛋白修饰在眼部疾病的研究进展

Research progress on protein glycosylation modification in ocular diseases

来源期刊： 眼科学报 | 2024年4月 第39卷 第4期： 220-228 发布时间： 收稿时间：2024/7/19 10:07:35 阅读量：703
作者：
郑竹卿,
李柯然,
柏文,
关键词：
糖基化翻译后修饰眼部疾病
glycosylation posttranslational modification ocular disease
DOI：
10.12419/24050603.
收稿时间：
2024-03-03 
修订日期：
2024-04-10 
接收日期：
2024-04-20 
糖基化是一种重要的蛋白质翻译后修饰，通常发生在内质网和高尔基体的特定位置。N-糖基化和O-糖基化是最常见的糖基化修饰类型。与其他翻译后修饰相比，糖基化具有独特的生物学意义，包括结构的复杂多样性，生物功能的重要性以及进化上的保守性。糖基化修饰对于蛋白质稳定性、细胞黏附与识别、细胞内信号传导和表观遗传学具有重要影响，从而参与调节细胞生物学和发病机制。近年来，越来越多的研究揭示了糖基化参与眼部疾病的发生和发展，包括眼表疾病、圆锥角膜、青光眼、年龄相关性黄斑变性、视网膜色素变性、糖尿病视网膜病变等。眼部蛋白糖基化异常可通过诱发新生血管形成、炎症反应、氧化应激、异常免疫应答等改变细胞的结构与功能，进而影响各种眼病的发生发展。通过深入研究糖基化在不同眼部疾病中的作用机制，可以为相关眼部疾病的早期诊断和治疗提供新的思路和方法。现综述糖基化在眼部疾病的研究进展，以探究调控蛋白质糖基化对眼部疾病的诊疗意义。
Glycosylation is an important post-translational modification of proteins that usually occurs at specific locations within the endoplasmic reticulum and Golgi apparatus. N-glycosylation and O-glycosylation are the most common types of glycosylation modifications. Compared to other post-translational modifications, glycosylation has unique biological significance, including structural complexity and diversity, crucial biological functions, and evolutionary conservation. Glycosylation modifications significantly impact protein stability, cell adhesion and recognition, intracellular signal transduction, and epigenetics, thereby regulating cellular biology and pathogenesis. In recent years, an increasing amount of research has revealed the involvement of glycosylation in the occurrence and development of ocular diseases, including ocular surface diseases, keratoconus, glaucoma, age-related macular degeneration, retinitis pigmentosa, and diabetic retinopathy. Abnormal glycosylation of ocular proteins can induce changes in cell structure and function through mechanisms such as neovascularization, inflammatory response, oxidative stress, and abnormal immune response, thereby influencing the occurrence and development of various eye diseases. By deeply studying the mechanisms of glycosylation in different ocular diseases, new insights and methods can be provided for the early diagnosis and treatment of related ocular diseases. This review summarizes the research progress of glycosylation in ocular diseases to explore the diagnostic and therapeutic significance of regulating protein glycosylation in ocular diseases.

文章亮点

1. 关键发现

糖基化修饰在眼部疾病的发生和进展中扮演了重要角色，涉及多种眼部疾病如眼表疾病、圆锥角膜、青光眼、年龄相关性黄斑变性、视网膜色素变性以及糖尿病视网膜病变等。
总结了糖基化在不同眼病发生发展中的病理过程和机制，揭示了这一过程如何影响眼部疾病的进展。

2. 已知与发现

糖基化修饰通过多种机制在细胞生物学和疾病机制中发挥作用。

3. 意义与改变

深入研究蛋白质糖基化的调控对眼部疾病的诊断和治疗具有重要意义，能够为相关眼病的早期检测和治疗提供新的策略和方法。

       糖基化是真核细胞中最为丰富和多样化的蛋白质翻译后修饰形式之一[1]。该过程起始于内质网，终止于高尔基体[2]，超过50%的蛋白质需要经过糖基化修饰，包括膜受体、黏附分子、细胞外基质蛋白、细胞内激酶和转录因子等。哺乳动物中最常见的糖基化修饰类型为N-糖基化和O-糖基化，广泛参与各项生理病理活动[3]。眼部蛋白的异常糖基化可以通过诱发新生血管形成、炎症反应、氧化应激、异常免疫应答等改变细胞的结构与功能，进而影响疾病的发生和发展。研究糖基化在眼部疾病病理改变中的作用将为疾病的诊疗提供新的方向和作用靶点，对于预防和揭示疾病的发生机制具有重要意义

1 糖基化特点及修饰种类

1.1 糖基化特点

       蛋白质糖基化是一个复杂的多步骤过程。糖基在一系列糖基转移酶和糖苷酶的作用下转移至蛋白质，和蛋白质上的氨基酸残基形成糖苷键，再经过一系列转运、剪切和修饰等过程完成糖蛋白的组装[3]。在蛋白质的多种翻译后修饰中，糖基化是普遍存在的一种重要类型。与其他翻译后修饰相比，糖基化具有独特的生物学意义。1)结构的复杂多样性：糖基化可以将复杂的糖链结构以不同方式连接到蛋白质上，从而使糖蛋白具有高度的结构异质性[4]，这种多样性超过了其他大多数翻译后修饰。2)生物功能的重要性：糖基化在细胞识别与通讯、信号传导与调控、蛋白质的折叠与稳定性方面具有独特的作用[5]。3)进化上的保守性：糖基化是高度保守的生物过程，在进化过程中具有重要功能，从简单的原核生物到复杂的哺乳动物，都具有类似的糖基化机制[6]。

1.2 糖基化类型

       根据糖蛋白中糖链与蛋白质的连接方式，糖基化可分为N-糖基化、O-糖基化、C-甘露糖基化、糖基磷脂酰肌醇锚区等[1]。鉴于N-糖基化和O-糖基化是最常见的糖基化修饰类型，以下内容将重点讨论这两种修饰在眼部疾病中的重要作用。
       1.2.1 O-糖基化
       O-糖基化修饰通常发生在蛋白质多肽链丝氨酸或苏氨酸的羧基上[7]。根据与蛋白质残基相连的单糖种类分为O-GlcNAc糖基化和黏蛋白型O-GalNAc糖基化两种形式[8]。前者通过O-GlcNAc糖基转移酶(O-GlcNAc transferase,OGT)和O-GlcNAc水解酶(O-GlcNAcase,OGA)进行调控[9]，后者通过N-乙酰氨基半乳糖转移酶家族调控[10]，整个过程发生在高尔基体中。其中，O-GlcNAc糖基化是指单糖分子N-乙酰葡萄糖胺(N-acetylglucosamine,GlcNAc)共价地连接到蛋白质的谷氨酸残基上，OGT负责把GlcNAc从糖基供体UDP-GlcNAc共价连接到蛋白上, 而OGA则把GlcNAc从蛋白上水解下来[9]。
       1.2.2 N-糖基化
       N-糖基化修饰发生在蛋白质的Asn-X-Ser/Thr位点(X为除脯氨酸外任一氨基酸)，通过α-甘露糖苷酶、N-乙酰氨基葡萄糖转移酶参与调控，整个过程起始于内质网，完成于高尔基体[3]。初始的核心N-糖基结构为五糖核心，即Man3-GlcNAc2-Asn。在此基础上，N-糖基化根据糖型的特点可被划分为3种类型：高甘露糖型、复杂型和杂合型。

1.3 糖基化的生物学作用

       糖基化对生物学的作用主要涉及蛋白质稳定性、细胞黏附与识别、细胞内信号传导以及表观遗传学调控：1)在蛋白质稳定性方面，糖基化通过改变电荷状态和折叠状态，影响蛋白质与其他分子或细胞结构的相互作用，增加构象和热力学稳定性[11]。同时，糖链覆盖蛋白质分子的降解位点，提高蛋白质对水解酶的抵抗力[11]。2)细胞表面的糖基化蛋白在细胞间相互作用和信号传递中发挥关键作用，影响细胞的黏附、迁移和发育[12]。特定糖基化蛋白亚结构修饰后，能启动特定黏附分子相互作用，影响蛋白质功能[13]。3)糖基化参与细胞内信号传导通路的调控，例如血管内皮生长因子[14](vascular endothelial growth factor,VEGF)、 血管生成素/酪氨酸激酶受体-2[15-16](angiopoietin/tyrosine kinase receptor-2,Ang/Tie2)、硫氧还蛋白互作蛋白/碳水化合物反应元件结合蛋白[17](thioredoxin-interacting protein/carbohydrate response element binding protein,TXNIP/ChREBP)等，影响视网膜血管的稳定性、通透性和炎症过程。4)最后糖基化还能通过影响DNA和染色质的结构与功能，调控基因的表达。在DNA甲基化中，糖基化是关键步骤，通过提供底物将脱氧核苷酸添加到甲基化位点，实现DNA线性信息向三维结构的转换[18]。总体而言，糖基化在细胞生物学中发挥多方面的调控作用，对多个生理和病理过程具有重要影响。

2 糖基化与眼部疾病

2.1 眼表疾病

       在解剖学上，眼表是由角膜、结膜、眼睑及其上方的睑板腺和泪腺等组成。由于长期暴露于各种环境刺激物、病原体和过敏原，眼表发展了成熟的免疫系统和屏障功能[19]。正常的糖基化对眼表的结构稳定性和屏障功能至关重要。泪膜是眼表的首道屏障。黏蛋白(Mucin,MUC)是泪膜的重要成分，由角膜结膜上皮细胞、结膜杯状细胞及泪器(包括泪腺和泪道)产生，具有清除异物、抗菌润滑等功能，是迄今为止发现的分子量最大且最高度糖基化的糖蛋白[20]。实验证明，N-糖基化在眼表黏蛋白的表位暴露、细胞内运输、抗黏附和屏障功能中发挥着重要作用[21]，其机制包括促进MUC16对半乳糖凝集素-3的结合亲和力，从而将凝集素保留在上皮细胞表面，促进角膜中保护性晶格的形成，以维持角膜上皮细胞的完整性和稳定性[21]。另外，泪液中高度O-糖基化的黏蛋白可以润滑眼表顶端边界、限制金黄色葡萄球菌对上皮细胞的黏附[22]、发挥免疫调节作用[23]以降低眼部感染损伤的风险。在生理状态下，角膜上皮表层细胞之间相互作用，形成了另一道具有选择性通透功能的屏障。在糖尿病患者中，O-GlcNAc和OGT的免疫反应活性过度增加，会导致角膜上皮基底层细胞中半桥粒数目减少，上皮基底膜与上皮基底层细胞的脱离，进而促使糖尿病角膜上皮损伤的发生[24]。此外，在干眼症和眼表炎症期间，角膜上皮O-糖基化发生动态变化，黏蛋白的表达、分泌及其聚糖结构受到影响[25-26]。轻中度干眼时MUC1的唾液酸化作用上调，而重度干眼时MUC1的唾液酸化作用下降[27]。糖基化紊乱与眼表疾病之间存在着密切关联，干预糖基化可能是减少眼表炎症和损伤的发生新型靶点。

2.2 圆锥角膜

       圆锥角膜是一种罕见且严重的眼病，角膜胶原数量和密度减少、基质层变薄是其组织学变化之一[28]。糖基化过程可以增强角膜交联，从而减少圆锥角膜的发病风险。多项研究发现，圆锥角膜与糖尿病之间存在负相关，原因在于糖尿病患者由于体内高水平的葡萄糖，导致角膜纤维的糖基化增强，从而诱导基质中的天然胶原交联[29-31]，使角膜硬化，增强角膜的生物力学和抗张强度，可控制圆锥角膜的发生和发展。然而当角膜糖基化异常，产生不同于正常角膜含量的糖残基，如N-乙酰-D-葡萄糖胺、L-岩藻糖和唾液酸等[32]，同样也可能导致上皮的形态功能发生变化，如变薄、断裂和各种黏附分子的表达异常等[33]，诱发角膜的结构改变，引起圆锥角膜。此外，在圆锥角膜的上皮细胞表面，发现了大量与半乳糖连接的非乙酰化唾液酸，Mencucci等[32]认为这可能是试图恢复正常上皮结构的一种补偿机制。然而，在圆锥角膜的鲍曼层或其缺陷区域，没有发现显著的糖基化变化[33]。这表明糖基化可能并非圆锥角膜结构变化的唯一决定因素，圆锥角膜结构可能受到多种特定因素的影响。未来，糖基化有望成为圆锥角膜的潜在诊断标志物及治疗靶点。

2.3 青光眼

       青光眼是一种复杂的多因素导致的眼部疾病，它是导致全球失明的主要原因之一。小梁网(trabecular meshwork,TM)是前房角处由胶原纤维构成的网状结构，它是眼房水排出的重要通路，该处的病理性改变可升高眼内压，导致青光眼的发生[34]。细胞表面蛋白糖基化和聚糖层充当流体剪切应力的传感器，起到传递机械感应、启动细胞骨架肌动蛋白网络中的响应作用[35]。TM细胞正是在不断受到不同水平的流体剪切应力的环境中发挥功能[36]，异常的糖基化可能会改变TM细胞承受流体剪切的能力，从而介导青光眼的病理学机制。Sienkiewicz等[37]研究发现，在原发性开角型青光眼和青少年青光眼中，TM的全局蛋白糖基化发生异常(同时发生低糖基化和高糖基化)，使用某些糖基化抑制剂后，TM细胞转运示踪剂减少，流出通道受阻，从而推断糖基化可以通过影响TM细胞形态、运动及其与基质的相互作用，改变细胞间隙的开放和关闭，控制TM中房水的流动。此外，一些高度糖基化的细胞外基质蛋白如Cochlin[38]、Versican[39]、透明质酸[40]，被发现存在于青光眼患者的TM中。它们的分布与流出阻力有关，起到调节流体通道的流动模式和TM刚度的作用[41]。然而具体的动力学机制以及发生改变的糖基化类型还不明晰，有待进一步研究。

2.4 年龄相关性黄斑变性

       年龄相关性黄斑变性(age-related macular degeneration, AMD)是老年人中最常见的致盲性疾病。糖基化异常提供了AMD病因学的新视角。AMD根据是否存在新生血管，分为干性和湿性。研究显示糖基化是AMD的相关影响因素，血小板反应蛋白(-1thrombospondin-1, TSP1)的C-甘露糖基化减少患干性AMD的风险[42]。干性AMD的特征是年龄相关的玻璃膜疣积累，其起源于已经发生视网膜色素上皮(retinal pigment epithelium,RPE)细胞退化并富含光感受器残留物的区域[43]。衰老能够引起多种糖基酶活性下降，如α-甘露糖苷酶、N-乙酰基-β-葡糖苷酶和β-半乳糖苷酶[44]，进而影响了光感受器圆盘外段中甘露糖、N-乙酰葡糖胺和半乳糖的降解，干扰了细胞代谢，从而引发了玻璃膜疣的异常积累[45-46]。此外，AMD患者的血浆糖组学[47]发现，单侧AMD疾病阶段表征免疫调节性的双天线聚糖结构(双触角IgG GP18)显著降低，而双侧疾病阶段表征炎症反应的四触角血浆聚糖13(digalactosylated tetraantennary glycan 13,DG13)大幅增加。表明血浆中免疫球蛋白聚糖结构改变引起的免疫调节失衡和炎症反应与AMD的进展相关。湿性AMD的特征是脉络膜新生血管(choroidal neovascularization,CNV)，尽管该过程也和炎症相关，然而目前暂无直接的糖生物学研究，糖基化与CNV之间的关系或许可以成为AMD病因学研究的未来方向。

2.5 视网膜色素变性

       视网膜色素变性(retinitis pigmentosa,RP)是一种遗传性视网膜变性疾病，其主要特征是进行性视网膜光感受器细胞凋亡和色素上皮变性[48]。在光感受器细胞中，多个位点都受到糖基化的调控，例如视紫红质的Asn2和Asn15位点[49]、红色和绿色视锥细胞视蛋白(hOPSR、hOPSG)的Asn34位点[50]等。糖基化有助于维持光感受器细胞的存活、稳定性以及视锥视杆蛋白的功能和形态。一些研究表明，糖基化缺陷与感光细胞异常、老化，以及感光细胞外节的膜吞噬功能受损有关，从而导致RP的发生[51]。视紫红质是视网膜杆状光感受器中最丰富的蛋白质之一，Murray等[52]通过表达非糖基化的视紫红质的转基因小鼠模型发现，这些小鼠的视杆细胞呈现外节的空泡化和形态扭曲。而表达携带T17M突变的人类视紫红质(human rhodopsin with a T17M mutation,hT17M)的转基因小鼠也出现了相似的外节空泡化，这表明糖基化缺陷在某些遗传突变引起的RP表型中可能起到一定的作用。此外，在人类先天性糖基化缺陷病例中也有发生RP的报道[53]，表明一些与糖基化相关的基因突变也直接导致RP的发生。例如O-甘露糖β1、2-N-乙酰氨基葡萄糖转移酶1的突变会引起视网膜色素变性RP76[54]，而SRD5A3基因突变以及其他糖基化紊乱相关基因的突变也可能导致早发性视网膜营养不良等视网膜疾病[55]。这些研究进一步强调了糖基化在RP的发病机制中的重要性，以及它与多种遗传和遗传突变引起的视网膜疾病之间的紧密联系。

2.6 糖尿病视网膜病变

       糖尿病性视网膜病变(diabetic retinopathy,DR)是糖尿病患者中常见的慢性并发症之一，也是成年人失明的主要原因[56]。DR的发病机制涉及多个方面，其中血管功能失调和炎症反应与病变的进展密切相关。
       血管功能失调在DR的病理过程中扮演着重要角色，包括血管新生、血管渗漏和周细胞丧失等。O-GlcNAc修饰在DR的病理过程中起到关键作用，通过影响关键分子和通路调节血管功能。高糖浓度环境下，视网膜细胞中的O-GlcNAc和OGT活性增强，继而增加VEGF的表达，促进视网膜微血管内皮细胞的激活、增殖和迁移[57-58]。相反，抑制视网膜血管内皮细胞的O-GlcNAc水平可以降低VEGF表达水平，从而抑制DR的发展[59]。另外，O-GlcNAc过度活化可以抑制FoxO1磷酸化，使其入核，以激活Ang-2表达[15-16]。过去的研究显示Ang-2能够在DR中引发血管问题，通过竞争性阻止Ang-1与Tie2结合，导致视网膜血管不稳定和通透性增加[60-62]。同时，O-GlcNAc过度活化可以调节VE-钙黏蛋白的磷酸化，导致内皮屏障丧失，从而增加血管通透性[63]。除了内皮细胞，周细胞也对维持视网膜血管的稳定性至关重要。在高血糖下，小鼠视网膜周细胞中许多参与程序性死亡的蛋白质被O-GlcNAc修饰[64]，p53便是其中之一。p53是周细胞凋亡的潜在关键蛋白，p53的O-GlcNAc修饰及其增加的水平将导致周细胞的早期丢失[64]。这种凋亡可能导致视网膜血管的不稳定性，从而促进DR的发展。
       炎症反应和氧化应激也与DR的发病机制紧密相关。研究表明，糖尿病患者视网膜中OGT的增加导致ChREBP和TXNIP水平上升，激活核因子-κB。同时，OGT还能促进ChREBP的O-GlcNAc修饰，共同发挥促炎作用[17]。此外，另一项研究发现，DR患者的IgG半乳糖基化、岩藻糖基化和唾液酸化水平降低，平分型N-乙酰葡糖胺修饰增加，从而导致视网膜IgG的抗体依赖性的细胞介导的细胞毒作用(antibody-dependent cell-mediated cytotoxicity,ADCC)和补体依赖的细胞毒性(complement dependent cytotoxicity,CDC)增强[65]。这加重了炎性反应和组织损伤，引发一系列病理改变。另一方面，O-GlcNAc的激活也被发现可以通过减少活性氧(reactive oxygen species,ROS)的产生、增加抗氧化基因的表达、维护线粒体膜电位、预防凋亡等机制对视网膜内皮细胞发挥保护作用[66]。这表明了糖基化在DR发病机制中的双重作用，一方面促进了病变，另一方面提供了一种保护机制。

3 临床潜力和应用

       在当前的医学研究中，糖基化是一个潜力巨大的研究领域，在诊断和治疗疾病方面展现出良好的应用前景。

3.1 疾病诊断

       不同眼部疾病中的差异糖基化模式可作为标志物，具有用于早期诊断、分型、疗效评估和疾病预后预测的潜力。与传统眼部影像学检查相比，糖基化标志物更具特异性和敏感性。在DR方面，Zhang等[67]的研究通过质谱法探讨了血浆IgG糖基化与DR的关系，其中7种糖肽比率能有效区分非增殖性糖尿病视网膜病变(non-proliferative diabetic retinopathy,NPDR)和无糖尿病视网膜病变(non-diabetic retinopathy,NDR)，具有较好的诊断能力。另外，Wu等[68]的研究发现2个IgG糖基峰(GP15、GP20)和2个衍生结构(IGP32、IGP54)与DR显著相关。检测这些标志物的水平，可能会在DR的早期诊断方面具有前瞻性作用。在AMD方面，血浆IgG免疫调节性双天线聚糖结构的含量降低以及促炎四触角血浆聚糖的含量增加，可能是AMD潜在的生物标志物[47]。除了血浆成分检测外，眼部体液检测也是诊断眼部疾病的重要方法，包括对泪液、房水和玻璃体液的成分分析、病原分离培养等[69]。由于技术复杂性和样本量限制，目前有关眼部体液的糖基化检测的研究较为缺乏。基于血浆糖基化蛋白检测的可行经验，随着未来高通量、高灵敏度的糖基化修饰检测技术的开发，眼部体液糖基化检测标准化流程的建立，有望实现对眼部异常糖基化位点和聚糖进行快速和精确的检测，为疾病病理生理机制研究、特异性诊断提供参考。

3.2 疾病治疗

       针对糖基化修饰治疗制剂的研发是眼部疾病研究的新方向。由于糖基化调控许多细胞信号通路和蛋白质的功能，针对糖基化靶点的抑制剂具有潜在的治疗前景。然而，在治疗制剂研发方面，目前仍然停留在对糖基化潜在治疗靶点的发现阶段。迄今为止，没有一种糖基化抑制剂获得临床应用许可。此外，糖基化修饰还可作为优化治疗性抗体的生产手段，用于提高抗VEGF抗体的药效和稳定性[1]。阿柏西普方案中眼压升高的发生率明显低于雷珠单抗方案。推测可能是因为阿柏西普在玻璃体内发生糖基化的缘故，有助于改善其在玻璃体腔内的溶解性，减少小梁网中蛋白质的
积累[70]。在眼部疾病，优化治疗性抗体具有潜在的应
用前景，值得进一步发掘。

4 小结与展望

       糖基化在生物学过程中扮演重要且多样的角色，涉及糖基化类型的改变、缺失、突变以及表达改变等，与多种眼部疾病的发生和发展密切相关。深入研究糖基化的机制，并寻找抑制糖基化过程的方法，对于预防和治疗眼部疾病具有重要意义。尽管糖基化在临床应用中具有巨大潜力，但仍然面临研究受限、检测技术不足、机制复杂需深入探究以及药物治疗仍处于起步阶段等多方面挑战。未来，随着糖组学技术的不断进步，将继续为这一领域带来革命性的变化，为眼部疾病的诊断、预后和治疗策略提供新的靶点。

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1、南京市医学科技发展项目(YKK23264)。
This work was supported by the Medical Technology Development Project of Nanjing, China(YKK23264).()
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