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A new insight into thymosin β4, a promising therapeutic approach for neurodegenerative disorders

机译:一个新的见解胸腺素β4,一种很有前途的治疗方法为神经退行性障碍

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Thymosin β4 (Tβ4), a G-actin-sequestering secreted peptide, improves neurovascular remodeling and central nervous system plasticity, which leads to neurological recovery in many neurological diseases. Inflammatory response adjustment and tissue inflammation consequences from neurological injury are vital for neurological recovery. The innate or nonspecific immune system is made of different components. The Toll-like receptor pro-inflammatory signaling pathway, which is one of these components, regulates tissue injury. The main component of the Toll-like/IL-1 receptor signaling pathway, which is known as IRAKI, can be regulated by miR-146a and regulates NF-kB expression. Due to the significant role of Tβ4 in oligoden-drocytes, neurons, and microglial cells in neurological recovery, it is suggested that Tβ4 regulates the Toll-like receptor (TLR) pro-inflammatory signaling pathway by upregulating miR-146a in neurological disorders. However, further investigations on the role of Tβ4 in regulating the expression of miR146a and TLR signaling pathway in the immune response adjustment in neurological disorders provides an insight into mechanisms of action and the possibility of Tβ4 therapeutic effect enhancement.
机译:胸腺素β4 (Tβ4)G-actin-sequestering分泌肽,提高神经与血管的重塑中枢神经系统可塑性,导致在许多神经神经复苏疾病。组织炎症的后果神经损伤神经系统是至关重要的复苏。是由不同的组件。受体促炎症信号通路,这是这些组件之一,调节组织损伤。toll样/ il - 1受体信号通路,被称为伊拉克人,可以由mir - 146 a和调节NF-kB表达式。重要的角色oligoden-drocytes Tβ4的神经元,神经和小胶质细胞恢复,建议Tβ4调节的toll样受体(TLR)促炎症信号通路的移植mir - 146 a神经障碍。调查在调节Tβ4的作用miR146a和TLR信号的表达在免疫反应调整路径神经系统疾病提供了一个洞察机制的行动和Tβ4的可能性治疗效果的提高。

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