Role of IL-17A in different stages of ischemic stroke

Role of IL-17A in different stages of ischemic stroke
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DOI:
10.1016/j.intimp.2023.109926
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发表时间:
2023-03-11
影响因子:
5.6
通讯作者:
Li, Hui
Li, Hui
中科院分区:
医学2区
文献类型:
--
作者:
Chen, Xiuping;Zhang, Yi;Li, Hui

文献摘要

被引文献

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白细胞介素-17A(IL-17 A)在缺血性脑卒中的发生发展中起重要作用。IL-17 A介导内皮炎症反应,促进水和钠潴留,改变心房的电生理结构,加速动脉粥样硬化斑块、高血压和房颤等缺血性中风危险因素的进展。在缺血性中风的急性期,IL-17 A通过中性粒细胞对损伤部位的趋化性、诱导神经元凋亡和激活钙蛋白酶-TRPC-6(瞬时受体电位通道-6)途径介导神经元损伤。在缺血性中风恢复期间,主要来源于反应性星形胶质细胞的IL-17 A促进和维持室下区(SVZ)神经前体细胞(NPC)的生存、神经元分化和突触形成,并参与神经功能的修复。针对IL-17 A相关炎症信号通路的治疗可以降低缺血性卒中和神经元损伤的风险,是缺血性卒中及其危险因素的新治疗策略。本文将简要讨论IL-17 A在缺血性卒中危险因素、急性和慢性炎症反应中的病理生理作用,以及靶向IL-17 A的潜在治疗价值。
Interleukin-17A (IL-17A) plays an important role in the progression of ischemic stroke. IL-17A mediates the endothelial inflammatory response, promotes water and sodium retention, and changes the electrophysiological structure of the atrium, accelerating the progression of ischemic stroke risk factors such as atherosclerotic pla-ques, hypertension, and atrial fibrillation. In the acute phase of ischemic stroke, IL-17A mediates neuronal injury through neutrophil chemotaxis to the site of injury, the induction of neuronal apoptosis, and activation of the calpain-TRPC-6 (transient receptor potential channel-6) pathway. During ischemic stroke recovery, IL-17A, which is mainly derived from reactive astrocytes, promotes and maintains the survival of neural precursor cells (NPCs) in the subventricular zone (SVZ), neuronal differentiation, and synapse formation and participates in the repair of neurological function. Therapies targeting IL-17A-associated inflammatory signaling pathways can reduce the risk of ischemic stroke and neuronal damage and are a new therapeutic strategy for ischemic stroke and its risk factors. In this paper, we will briefly discuss the pathophysiological role of IL-17A in ischemic stroke risk factors, acute and chronic inflammatory responses, and the potential therapeutic value of targeting IL-17A.