Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.
Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.
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多发性硬化症(MS)是一种慢性自身免疫性中枢神经系统(CNS)炎症性脱髓鞘疾病，由针对少突胶质细胞和髓鞘的自身免疫攻击引发。最近的研究表明，自身免疫攻击导致的少突胶质细胞的死亡在MS及其动物模型实验性自身免疫性脑脊髓炎(EAE)的发病机制中起着重要作用。多发性硬化症研究中的一个关键挑战在于了解控制少突胶质细胞存活的机制，并设计出提高少突胶质细胞存活的治疗方法。在这里，我们提供了最近的发现，强调了少突胶质细胞死亡对MS和EAE的发展的贡献，并总结了目前关于这些疾病中少突胶质细胞存活机制的文献。
Multiple sclerosis (MS) is a chronic autoimmune inflammatory demyelinating disease of the central nervous system (CNS), which is triggered by an autoimmune assault targeting oligodendrocytes and myelin. Recent research indicates that the demise of oligodendrocytes due to an autoimmune attack contributes significantly to the pathogenesis of MS and its animal model experimental autoimmune encephalomyelitis (EAE). A key challenge in MS research lies in comprehending the mechanisms governing oligodendrocyte viability and devising therapeutic approaches to enhance oligodendrocyte survival. Here, we provide an overview of recent findings that highlight the contributions of oligodendrocyte death to the development of MS and EAE and summarize the current literature on the mechanisms governing oligodendrocyte viability in these diseases.
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影响因子：
12.7
作者：
Bradl M;Lassmann H
通讯作者：
Lassmann H
DOI：
10.1126/science.aaa4484
发表时间：
2015-04-10
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Das I;Krzyzosiak A;Schneider K;Wrabetz L;D'Antonio M;Barry N;Sigurdardottir A;Bertolotti A
通讯作者：
Bertolotti A
影响因子：
2.3
作者：
Fortunato, Giuliana;Calcagno, Giuseppe;Sacchetti, Lucia
通讯作者：
Sacchetti, Lucia
影响因子：
5.3
作者：
Balabanov, Roumen;Strand, Krystle;Popko, Brian
通讯作者：
Popko, Brian
影响因子：
9.3
作者：
Castellazzi, Massimiliano;Patergnani, Simone;Pinton, Paolo
通讯作者：
Pinton, Paolo