Blockage of MLKL prevents myelin damage in experimental diabetic neuropathy.
Jia GuoZehui GuoYanju HuangSuchen MaBo YanChenjie PanZhaodi JiangFengchao WangZhiyuan ZhangYuwei DaXiaodong WangZhengxin YingPublished in: Proceedings of the National Academy of Sciences of the United States of America (2022)
SignificanceDiabetic neuropathy is a commonly occurring complication of diabetes that affects hundreds of millions of patients worldwide. Patients suffering from diabetic neuropathy experience abnormal sensations and have damage in their peripheral nerve axons as well as myelin, a tightly packed Schwann cell sheath that wraps around axons to provide insulation and increases electrical conductivity along the nerve fibers. The molecular events underlying myelin damage in diabetic neuropathy are largely unknown, and there is no efficacious treatment for the disease. The current study, using a diabetic mouse model and human patient nerve samples, uncovered a molecular mechanism underlying myelin sheath damage in diabetic neuropathy and provides a potential treatment strategy for the disease.
Keyphrases
- peripheral nerve
- type diabetes
- end stage renal disease
- mouse model
- wound healing
- oxidative stress
- newly diagnosed
- ejection fraction
- chronic kidney disease
- white matter
- cardiovascular disease
- peritoneal dialysis
- prognostic factors
- endothelial cells
- adipose tissue
- mesenchymal stem cells
- metabolic syndrome
- patient reported outcomes
- multiple sclerosis
- combination therapy
- bone marrow
- case report
- induced pluripotent stem cells