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Thymosin beta 4 as a restorative/regenerative therapy for neurological injury and neurodegenerative disease

机译:胸腺素β4作为神经损伤和神经退行性疾病的修复/再生疗法

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摘要

Thymosin beta 4 (T beta 4) promotes CNS and peripheral nervous system (PNS) plasticity and neurovascular remodeling leading to neurological recovery in a range of neurological diseases. Treatment of neural injury and neurodegenerative disease 24 h or more post-injury and disease onset with T beta 4 enhances angiogenesis, neurogenesis, neurite and axonal outgrowth, and oligodendrogenesis, and thereby, significantly improves functional and behavioral outcomes. We propose that oligodendrogenesis is a common link by which T beta 4 promotes recovery after neural injury and neurodegenerative disease. The ability to target many diverse restorative processes via multiple molecular pathways that drive oligodendrogenesis and neurovascular remodeling may be mediated by the ability of T beta 4 to alter cellular expression of microRNAs (miRNAs). However, further investigations on the essential role of nniRNAs in regulating protein expression and the remarkable exosomal intercellular communication network via exosomes will likely provide insight into mechanisms of action and means to amplify the therapeutic effects of T beta 4.
机译:胸腺素beta 4(T beta 4)促进中枢神经系统和周围神经系统(PNS)的可塑性和神经血管重构,从而导致一系列神经系统疾病的神经系统恢复。神经损伤和神经退行性疾病的治疗在受伤后24小时或更长时间以及使用T beta 4发作的疾病可增强血管生成,神经发生,神经突和轴突生长以及少突胶质生成,从而显着改善功能和行为结局。我们建议少突胶质生成是Tβ4促进神经损伤和神经退行性疾病后恢复的共同纽带。 T beta 4改变microRNA(miRNA)细胞表达的能力可以介导通过驱动少突胶质形成和神经血管重塑的多种分子途径靶向多种多样的修复过程的能力。但是,进一步研究nniRNA在调节蛋白表达中的基本作用以及通过外泌体产生的显着的外泌体细胞间通讯网络,可能会提供作用机制和扩大T beta 4疗效的手段的见解。

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