4.6 Article

Inflammation: Therapeutic Targets for Diabetic Neuropathy

Journal

MOLECULAR NEUROBIOLOGY
Volume 49, Issue 1, Pages 536-546

Publisher

HUMANA PRESS INC
DOI: 10.1007/s12035-013-8537-0

Keywords

Inflammatory cytokine; Adhesion molecule; Chemokine; Diabetic neuropathy; Pathways; Anti-inflammation

Categories

Funding

  1. National Natural Science Foundation of China [81100597]
  2. Natural Science Foundation Project of the Chongqing Science and Technology Commission (CSTC) [2009BA5012]
  3. Natural Science Foundation of the Third Military Medical University [2012XJQ17, 2009XQN34]

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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.

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