髓鞘
视神经
少突胶质细胞
生物
神经科学
糖尿病
再髓鞘化
视神经病变
糖尿病性视网膜病变
中枢神经系统
内分泌学
作者
Haoqian Wu,Xianjun Chen,Bin Yu,Jieqiong Zhang,Xingmei Gu,Wei Liu,Feng Mei,Jian Ye,Lan Xiao
出处
期刊:Glia
[Wiley]
日期:2023-01-20
卷期号:71 (5): 1333-1345
被引量:2
摘要
Visual impairment in diabetes is a growing public health concern. Apart from the well-defined diabetic retinopathy, disturbed optic nerve function, which is dependent on the myelin sheath, has recently been recognized as an early feature of visual impairment in diabetes. However, the underlying cellular mechanisms remain unclear. Using a streptozotocin-induced diabetic mouse model, we observed a myelin deficiency along with a disturbed composition of oligodendroglial lineage cells in diabetic optic nerve. We found that new myelin deposition, a continuous process that lasts throughout adulthood, was diminished during pathogenesis. Genetically dampening newly generated myelin by conditionally deleting olig2 in oligodendrocyte precursor cells within this short time window extensively delayed the signal transmission of the adult optic nerve. In addition, clemastine, an antimuscarinic compound that enhances myelination, significantly restored oligodendroglia, and promoted the functional recovery of the optic nerve in diabetic mice. Together, our results point to the role of new myelin deposition in optic neuropathy under diabetic insult and provide a promising therapeutic target for restoring visual function.
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