Inflammation: Therapeutic Targets for Diabetic Neuropathy

被引:85
|
作者
Zhou, Jiyin [1 ]
Zhou, Shiwen [1 ]
机构
[1] Third Mil Med Univ, Xinqiao Hosp, Natl Drug Clin Trial Inst, Chongqing 400037, Peoples R China
基金
中国国家自然科学基金;
关键词
Inflammatory cytokine; Adhesion molecule; Chemokine; Diabetic neuropathy; Pathways; Anti-inflammation; CYCLOOXYGENASE-2 GENE INACTIVATION; C-REACTIVE PROTEIN; PERIPHERAL NEUROPATHY; SCIATIC-NERVE; ADHESION MOLECULES; MOUSE MODEL; TNF-ALPHA; SUPRASCAPULAR NEUROPATHY; ANTIOXIDANT MECHANISMS; NITROSATIVE STRESS;
D O I
10.1007/s12035-013-8537-0
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
There are still no approved treatments for the prevention or of cure of diabetic neuropathy, and only symptomatic pain therapies of variable efficacy are available. Inflammation is a cardinal pathogenic mechanism of diabetic neuropathy. The relationships between inflammation and the development of diabetic neuropathy involve complex molecular networks and processes. Herein, we review the key inflammatory molecules (inflammatory cytokines, adhesion molecules, chemokines) and pathways (nuclear factor kappa B, JUN N-terminal kinase) implicated in the development and progression of diabetic neuropathy. Advances in the understanding of the roles of these key inflammatory molecules and pathways in diabetic neuropathy will facilitate the discovery of the potential of anti-inflammatory approaches for the inhibition of the development of neuropathy. Specifically, many anti-inflammatory drugs significantly inhibit the development of different aspects of diabetic neuropathy in animal models and clinical trials.
引用
收藏
页码:536 / 546
页数:11
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