Thyroid Hormone Potentially Benefits Multiple Sclerosis via Facilitating Remyelination

Thyroid Hormone Potentially Benefits Multiple Sclerosis via Facilitating Remyelination
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甲状腺激素通过促进髓鞘再生可能有益于多发性硬化症

DOI:
10.1007/s12035-015-9375-z
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发表时间:
2016-09
影响因子:
5.1
通讯作者:
Yao Zhongxiang
Yao Zhongxiang
中科院分区:
医学2区
文献类型:
--
作者:
Zhang Mao;Ma Ziyi;Qin Haochen;Yao Zhongxiang

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多发性硬化症(MS)是一种影响中枢神经系统(CNS)的常见自身免疫性疾病,少突胶质细胞(OLs)炎性损伤并伴有轴突变性所致的髓鞘破坏是多发性硬化症(MS)的主要组织病理学特征之一。在过去的20多年里,治疗主要集中在免疫系统,更具体地说,是对免疫细胞行为的调节。它似乎对复发的MS有效,而对于脱髓鞘后的神经变性超过炎症的进展性MS几乎没有好处。另外,由少突胶质前体细胞(OPC)产生的少突胶质细胞所产生的再髓鞘作用被认为是治疗进展性MS的潜在靶点。在本文中,鉴于甲状腺激素(TH)所起的关键作用,再髓鞘作用在MS中的积极作用将被讨论,主要集中在以下几点:(1)TH对MS潜在的再髓鞘作用;(2)TH能够促进再髓鞘形成的积极作用;(3)TH对内源性干细胞和前体细胞的调节作用;(4)TH对基因转录的影响;(5)一种工作假说,即TH可以通过促进再髓鞘形成来缓解MS,其机制是调节OPC的基因转录。
Myelin destruction due to inflammatory damage of oligodendrocytes (OLs) in conjunction with axonal degeneration is one of the major histopathological hallmarks of multiple sclerosis (MS), a common autoimmune disorder affecting the central nervous system (CNS). Therapies over the last 20 years mainly focus on the immune system and, more specifically, on the modulation of immune cell behavior. It seems to be effective in MS with relapse, while it is of little benefit to progressive MS in which neurodegeneration following demyelination outweighs inflammation. Otherwise, remyelination, as a result of oligodendrocyte production from oligodendrocyte precursor cells (OPCs), is considered to be a potential target for the treatment of progressive MS. In this review, positive effects of remyelination on MS will be discussed in view of the critical role played by thyroid hormone (TH), focusing on the following points: (1) promising treatment of TH on MS that potentially targets to remyelination; (2) the active role of TH that is able to promote remyelination; (3) the regulative role of TH that works on endogenous stem and precursor cells; (4) the effect of TH on gene transcription; and (5) a working hypothesis which is developed that TH can alleviate MS by promoting remyelination, and the mechanism of which is its regulative role in gene transcription of OPCs.
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