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The role of neurogenesis in neurorepair after ischemic stroke

机译:神经发生在缺血性卒中后神经皮病原体的作用

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Stroke consists of an abrupt reduction of cerebral blood flow resulting in hypoxia that triggers an excitotoxicity, oxidative stress, and neuroinflammation. After the ischemic process, neural precursor cells present in the subventricular zone of the lateral ventricle and subgranular zone of the dentate gyrus proliferate and migrate towards the lesion, contributing to the brain repair. The neurogenesis is induced by signal transduction pathways, growth factors, attractive factors for neuroblasts, transcription factors, pro and anti-inflammatory mediators and specific neurotransmissions. However, this endogenous neurogenesis occurs slowly and does not allow a complete restoration of brain function. Despite that, understanding the mechanisms of neurogenesis could improve the therapeutic strategies for brain repair. This review presents the current knowledge about brain repair process after stroke and the perspectives regarding the development of promising therapies that aim to improve neurogenesis and its potential to form new neural networks.
机译:中风由脑血流量突然降低导致缺氧,触发兴奋毒性,氧化应激和神经炎症。在缺血过程之后,牙齿侧脑室的腔内区中存在的神经前体细胞具有牙齿肠道的腔内区域,并朝向病变迁移,有助于脑修复。神经发生是通过信号转导途径,生长因子,神经细胞,转录因子,亲和抗炎介质和特异性神经递质的吸引因素诱导的神经发生。然而,这种内源性神经发生缓慢发生并且不允许完全恢复脑功能。尽管如此,了解神经发生的机制可以改善脑修复的治疗策略。本综述提出了关于中风后大脑修复过程的知识以及关于开发有前途的疗法的观点,旨在改善神经发生的疗法及其形成新神经网络的潜力。

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