The possible therapeutic role of advanced glycation end-product inhibitors in ischemic stroke

IF 3.7 3区医学 Q2 NEUROSCIENCES Brain Research Bulletin Pub Date : 2025-03-01 Epub Date: 2025-01-30 DOI:10.1016/j.brainresbull.2025.111236

Nada H. Aljarba , Hayder M. Al-Kuraishy , Ali I. Al-Gareeb , Mustafa M. Shokr , Marios Papadakis , Athanasios Alexiou , Mubarak Alruwaili , Mohammed Alrouji , Mohammed S. Alshammari , Gaber El-Saber Batiha

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Abstract

The advanced glycation end-products (AGEs) are toxic molecules result from non-enzymatic interactions of sugar with lipids or proteins. AGEs promote the generation of reactive oxygen species that induce the release of pro-inflammatory cytokines, and alter the intracellular signaling leading to progressive biochemical and metabolic derangements. AGEs-induced cellular aging is implicated in the development and progression of different neurological disorders such as dementia, neuropsychiatric disorders, and cerebrovascular diseases. Particularly, AGEs-induced microangiopathy and macroangiopathy trigger the induction of prothrombotic/thrombotic cascades with subsequent increase risk of acute ischemic stroke (AIS). Many studies highlighted that AGEs serum levels are correlated with the incidence, pathogenicity, and severity of AIS. However, the relationship between AGEs and AIS is not elucidated completely. Therefore, this review aims to discuss how AGEs promote the development and progression of AIS, and how AGEs inhibitors could be effective in the management of AIS.

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晚期糖基化终产物抑制剂在缺血性卒中中的可能治疗作用。

晚期糖基化终产物（AGEs）是糖与脂质或蛋白质非酶相互作用产生的有毒分子。AGEs促进活性氧的产生，从而诱导促炎细胞因子的释放，并改变细胞内信号，导致进行性生化和代谢紊乱。年龄诱导的细胞衰老涉及不同神经系统疾病的发生和进展，如痴呆、神经精神疾病和脑血管疾病。特别是，年龄诱导的微血管病变和大血管病变触发血栓形成/血栓形成级联反应，随后增加急性缺血性卒中（AIS）的风险。许多研究强调AGEs血清水平与AIS的发病率、致病性和严重程度相关。然而，AGEs与AIS之间的关系尚不完全清楚。因此，本文旨在探讨AGEs如何促进AIS的发展和进展，以及AGEs抑制剂如何有效地治疗AIS。

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来源期刊

Brain Research Bulletin 医学-神经科学

CiteScore

6.90

自引率

2.60%

发文量

253

审稿时长

67 days

期刊介绍： The Brain Research Bulletin (BRB) aims to publish novel work that advances our knowledge of molecular and cellular mechanisms that underlie neural network properties associated with behavior, cognition and other brain functions during neurodevelopment and in the adult. Although clinical research is out of the Journal''s scope, the BRB also aims to publish translation research that provides insight into biological mechanisms and processes associated with neurodegeneration mechanisms, neurological diseases and neuropsychiatric disorders. The Journal is especially interested in research using novel methodologies, such as optogenetics, multielectrode array recordings and life imaging in wild-type and genetically-modified animal models, with the goal to advance our understanding of how neurons, glia and networks function in vivo.