The Possible Role of Neural Cell Apoptosis in Multiple Sclerosis.
The Possible Role of Neural Cell Apoptosis in Multiple Sclerosis.
复制标题
神经细胞凋亡在多发性硬化中的作用。
DOI：
10.3390/ijms23147584
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发表时间：
2022-07-08
影响因子：
5.6
通讯作者：
Yu, Xiaoli
中科院分区：
文献类型：
--
作者：
Kennedy, Peter G. E.;George, Woro;Yu, Xiaoli
关键词：
多发性硬化症（MS）是一种影响中枢神经系统（CNS）的脱髓鞘疾病，其病因仍不清楚。虽然在MS病变中观察到少突胶质细胞和神经元的凋亡，但这种细胞死亡过程对疾病发病机制的贡献仍然存在争议。通常认为MS相关的脱髓鞘和轴突变性是神经炎症和靶向髓鞘蛋白的自身免疫过程的结果。然而，实验数据表明，少突胶质细胞和/或神经元细胞死亡可能确实先于炎症和自身免疫的发展。这些发现提出了一个问题，神经细胞凋亡是否是启动和/或驱动病理级联反应的关键事件，导致MS的临床功能缺陷。同样，关于轴突损伤，MS病变的一个关键病理特征，炎症独立和细胞自主神经元过程的作用需要进一步探讨。虽然MS中的少突胶质细胞和神经元损失可能不一定是相互排斥的，但应特别注意神经元凋亡在轴突损失发展中的作用。如果得到证实，多发性硬化症可以主要被视为一种神经退行性疾病，伴有继发性神经炎症和自身免疫过程。
The etiology of multiple sclerosis (MS), a demyelinating disease affecting the central nervous system (CNS), remains obscure. Although apoptosis of oligodendrocytes and neurons has been observed in MS lesions, the contribution of this cell death process to disease pathogenesis remains controversial. It is usually considered that MS-associated demyelination and axonal degeneration result from neuroinflammation and an autoimmune process targeting myelin proteins. However, experimental data indicate that oligodendrocyte and/or neuronal cell death may indeed precede the development of inflammation and autoimmunity. These findings raise the question as to whether neural cell apoptosis is the key event initiating and/or driving the pathological cascade, leading to clinical functional deficits in MS. Similarly, regarding axonal damage, a key pathological feature of MS lesions, the roles of inflammation-independent and cell autonomous neuronal processes need to be further explored. While oligodendrocyte and neuronal loss in MS may not necessarily be mutually exclusive, particular attention should be given to the role of neuronal apoptosis in the development of axonal loss. If proven, MS could be viewed primarily as a neurodegenerative disease accompanied by a secondary neuroinflammatory and autoimmune process.
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影响因子：
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