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κ 阿片受体与少突胶质细胞髓鞘再生。

Kappa opioid receptor and oligodendrocyte remyelination.

机构信息

Department of Histology and Embryology, Brain Science Key Laboratory of Chongqing Education Commission, Third Military Medical University, Chongqing, China.

Department of Histology and Embryology, Brain Science Key Laboratory of Chongqing Education Commission, Third Military Medical University, Chongqing, China.

出版信息

Vitam Horm. 2019;111:281-297. doi: 10.1016/bs.vh.2019.05.004. Epub 2019 Jun 28.

Abstract

Adult oligodendrocyte precursor cells (OPCs) maintain the abilities to differentiate and myelinate denuded axons in demyelinating diseases, such as Multiple Sclerosis (MS), albert often inefficiently. Remyelination therapies seek to enhance endogenous remyelination and represent a promising approach to achieve functional and cellular architectural recovery against neuronal deficits. Recent findings indicate that the kappa opioid receptor (KOR), a G-protein coupled receptor (GPCR), plays an important role in regulating oligodendrocyte differentiation and myelination. In this chapter, we reviewed (1) current knowledge of the functional importance of remyelination in demyelination diseases; (2) the opioids that can alter oligodendroglial proliferation and differentiation; (3) the endogenous KOR signaling in regulating oligodendrocyte myelination.

摘要

成体少突胶质前体细胞(OPC)在脱髓鞘疾病(如多发性硬化症)中保持分化和髓鞘形成裸露轴突的能力,但通常效率低下。髓鞘修复疗法旨在增强内源性髓鞘修复,是实现对抗神经元缺陷的功能和细胞结构恢复的有前途的方法。最近的研究结果表明,κ 阿片受体(KOR)是一种 G 蛋白偶联受体(GPCR),在调节少突胶质细胞分化和髓鞘形成方面发挥着重要作用。在本章中,我们回顾了(1)髓鞘修复在脱髓鞘疾病中的功能重要性的现有知识;(2)改变少突胶质细胞增殖和分化的阿片类药物;(3)内源性 KOR 信号在调节少突胶质细胞髓鞘形成中的作用。

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