期刊
DIABETES
卷 68, 期 11, 页码 2120-2130出版社
AMER DIABETES ASSOC
DOI: 10.2337/db18-1233
关键词
-
资金
- National Natural Science Foundation of China [31630037, 91740103, 31470768, 31670830]
- National Key R&D Program of China [2018YFA0800603]
- National Basic Research Program of China [2014CB542300]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDB19000000]
- Frontier Science of Chinese Academy of Sciences Key Research Projects [QYZDJ-SSW-SMC022]
- CAS/SAFEA International Partnership Program for Creative Research Teams
Diabetic peripheral neuropathy (DPN) is the most common complication in both type 1 and type 2 diabetes, but any treatment toward the development of DPN is not yet available. Axon degeneration is an early feature of many peripheral neuropathies, including DPN. Delay of axon degeneration has beneficial effects on various neurodegenerative diseases, but its effect on DPN is yet to be elucidated. Deficiency of Sarm1 significantly attenuates axon degeneration in several models, but the effect of Sarm1 deficiency on DPN is still unclear. In this study, we show that Sarm1 knockout mice exhibit normal glucose metabolism and pain sensitivity, and deletion of the Sarm1 gene alleviates hypoalgesia in streptozotocin-induced diabetic mice. Moreover, Sarm1 gene deficiency attenuates intraepidermal nerve fiber loss in footpad skin; alleviates axon degeneration, the change of g-ratio in sciatic nerves, and NAD(+) decrease; and relieves axonal outgrowth retardation of dorsal root ganglia from diabetic mice. In addition, Sarm1 gene deficiency markedly diminishes the changes of gene expression profile induced by streptozotocin in the sciatic nerve, especially some abundant genes involved in neurodegenerative diseases. These findings demonstrate that Sarm1 gene deficiency attenuates DPN in mice and suggest that slowing down axon degeneration is a potential promising strategy to combat DPN.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据