干细胞在脑卒中后神经可塑性中的作用机制

IF 0.7 Q4 PHARMACOLOGY & PHARMACY
Sri Yani, Jeanne Pawitan
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引用次数: 0

摘要

中风是世界上第二大可能导致永久性残疾的死亡原因。近年来,干细胞治疗缺血性脑卒中取得了很大进展。目前,已经有几项关于中风干细胞治疗的研究表明,使用不同的细胞来源和移植程序可以提高神经可塑性,但其机制仍然存在争议。因此,本综述的目的是分析干细胞增强神经可塑性的各种机制。干细胞增加神经可塑性的机制可以通过多种信号通路,即内皮素-3/EDNRB、sry相关的HMG-box 10 (SOX10)、Wnt/β-Catenin、GF1R+和C-X-C趋化因子受体4型(CXCR4)通路,以及通过神经营养因子(NT-3)、特化细胞外基质神经周围网络(ECM PNN)、microRNA (miR-133b和Ex-miR-17-92+簇)、以及磷酸化的塌陷蛋白反应介质蛋白2 (CRMP2)和磷酸化camp反应元件结合蛋白(p-CREB)、生长相关蛋白43 (GAP-43)和突触素(SYP)的调节增加。综上所述,多种信号通路和其他因素有助于中风干细胞治疗后神经可塑性的增强。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stem cell mechanism of action in neuroplasticity after stroke
Stroke is the second leading cause of death in the world that may cause a permanent disability. In recent years, stem cell therapy for ischemic stroke has made great progress. Currently, there have been several studies on stem cell therapy in stroke that provide benefits for neuroplasticity using various cell sources and transplant procedures, but the mechanisms are still controversial. Therefore, the aim of this review was to analyze the various mechanisms of stem cells in enhancing neuroplasticity. Stem cell mechanism that increases neuroplasticity can be through various signaling pathways, namely the endothelin-3/EDNRB, SRY-related HMG-box 10 (SOX10), Wnt/β-Catenin, GF1R+ and C-X-C chemokine receptor type 4 (CXCR4) pathways, and through neurotrophic factor (NT-3), specialized extracellular matrix perineuronal net (ECM PNN), microRNA (miR-133b and Ex-miR-17-92+ cluster), as well as modulation of proteins namely phosphorylated collapsin response mediator protein 2 (CRMP2) and increased regulation of phosphorylated-cAMP response element-binding protein (p-CREB), growth associated protein 43 (GAP-43), and synaptophysin (SYP). In conclusion, various signaling pathways and other factors contribute in neuroplasticity increase due to stem cell therapy in stroke.
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来源期刊
Egyptian Pharmaceutical Journal
Egyptian Pharmaceutical Journal PHARMACOLOGY & PHARMACY-
CiteScore
1.10
自引率
0.00%
发文量
37
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