期刊
PHARMACOLOGY & THERAPEUTICS
卷 120, 期 1, 页码 1-34出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pharmthera.2008.05.005
关键词
Diabetic neuropathy; Mitochondria; Oxidative stress; Pain therapy; Bioinformatics
资金
- NIH [T32 D07245]
- Juvenile Diabetes Research Foundation Center for the Study of Complications in Diabetes
- Program for Neurological Research and Development (PNRD)
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [T32DK007245] Funding Source: NIH RePORTER
Neuropathy is the most common and debilitating complication of diabetes and results in pain, decreased motility, and amputation. Diabetic neuropathy encompasses a variety of forms whose impact ranges from discomfort to death. Hyperglycemia induces oxidative stress in diabetic neurons and results in activation of multiple biochemical pathways. These activated pathways are a major source of damage and are potential therapeutic targets in diabetic neuropathy. Though therapies are available to alleviate the symptoms of diabetic neuropathy, few options are available to eliminate the root causes. The immense physical, psychological, and economic cost of diabetic neuropathy underscore the need for causally targeted therapies. This review covers the pathology, epidemiology, biochemical pathways, and prevention of diabetic neuropathy, as well as discusses current symptomatic and causal therapies and novel approaches to identify therapeutic targets. (c) 2008 Elsevier Inc. All rights reserved.
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