Department of Pharmacy & Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, 100029, People's Republic of China.
School of Life Sciences, Beijing University of Chinese Medicine, Beijing, 100029, People's Republic of China.
Neurochem Int. 2020 Jun;136:104731. doi: 10.1016/j.neuint.2020.104731. Epub 2020 Mar 19.
Increasing evidences support that glial connexins are involved in the demyelination pathology of multiple sclerosis (MS), a chronic inflammatory demyelinating disorder. Here, we review the data from patients with MS and animal models of MS that implicate connexins in demyelination. Connexins expressed in oligodendrocytes and astrocytes show diverse changes at the different phases of MS. Loss of oligodendrocyte or astrocyte connexins contributes to demyelination and exaggerates the pathology of MS. Channel-dependent and -independent connexins are involved in the pathology of demyelination, which is related with myelin integrity, metabolic homeostasis, the brain-blood barrier, the immune cell infiltration, and the inflammatory response. A comprehensive understanding of connexin function in demyelination may provide new therapeutic targets for MS.
越来越多的证据表明,神经胶质连接蛋白参与了多发性硬化症(MS)的脱髓鞘病理过程,这是一种慢性炎症性脱髓鞘疾病。在这里,我们综述了来自多发性硬化症患者和多发性硬化症动物模型的数据,这些数据表明连接蛋白在脱髓鞘中起作用。少突胶质细胞和星形胶质细胞中表达的连接蛋白在 MS 的不同阶段表现出不同的变化。少突胶质细胞或星形胶质细胞连接蛋白的缺失导致脱髓鞘,并加重 MS 的病理。依赖通道和不依赖通道的连接蛋白都参与了脱髓鞘的病理过程,这与髓鞘完整性、代谢稳态、血脑屏障、免疫细胞浸润和炎症反应有关。全面了解连接蛋白在脱髓鞘中的作用可能为多发性硬化症提供新的治疗靶点。