Li Jianzhuang, Qiu Yanmei, Zhang Chunlin, Wang Hailing, Bi Rentang, Wei Yanhao, Li Yanan, Hu Bo
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Pharmacol Res. 2023 May;191:106726. doi: 10.1016/j.phrs.2023.106726. Epub 2023 Mar 11.
Acute ischemic stroke (AIS) is a serious and life-threatening disease worldwide. Despite thrombolysis or endovascular thrombectomy, a sizeable fraction of patients with AIS have adverse clinical outcomes. In addition, existing secondary prevention strategies with antiplatelet and anticoagulant drugs therapy are not able to adequately decrease the risk of ischemic stroke recurrence. Thus, exploring novel mechanisms for doing so represents an urgent need for the prevention and treatment of AIS. Recent studies have discovered that protein glycosylation plays a critical role in the occurrence and outcome of AIS. As a common co- and post-translational modification, protein glycosylation participates in a wide variety of physiological and pathological processes by regulating the activity and function of proteins or enzymes. Protein glycosylation is involved in two causes of cerebral emboli in ischemic stroke: atherosclerosis and atrial fibrillation. Following ischemic stroke, the level of brain protein glycosylation becomes dynamically regulated, which significantly affects stroke outcome through influencing inflammatory response, excitotoxicity, neuronal apoptosis, and blood-brain barrier disruption. Drugs targeting glycosylation in the occurrence and progression of stroke may represent a novel therapeutic idea. In this review, we focus on possible perspectives about how glycosylation affects the occurrence and outcome of AIS. We then propose the potential of glycosylation as a therapeutic drug target and prognostic marker for AIS patients in the future.
急性缺血性卒中（AIS）是一种在全球范围内严重且危及生命的疾病。尽管有溶栓或血管内取栓治疗，但仍有相当一部分AIS患者出现不良临床结局。此外，现有的抗血小板和抗凝药物二级预防策略并不能充分降低缺血性卒中复发的风险。因此，探索新的机制来预防和治疗AIS迫在眉睫。最近的研究发现，蛋白质糖基化在AIS的发生和转归中起关键作用。作为一种常见的共翻译和翻译后修饰，蛋白质糖基化通过调节蛋白质或酶的活性和功能参与多种生理和病理过程。蛋白质糖基化与缺血性卒中脑栓塞的两个病因有关：动脉粥样硬化和心房颤动。缺血性卒中后，脑蛋白质糖基化水平受到动态调节，通过影响炎症反应、兴奋性毒性、神经元凋亡和血脑屏障破坏，显著影响卒中结局。针对卒中发生和进展过程中糖基化的药物可能代表一种新的治疗思路。在这篇综述中，我们重点探讨糖基化如何影响AIS的发生和转归的可能观点。然后，我们提出糖基化作为未来AIS患者治疗药物靶点和预后标志物的潜力。
