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Inflammation: Therapeutic Targets for Diabetic Neuropathy

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Abstract

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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Acknowledgments

The work was supported by grants from the National Natural Science Foundation of China (no. 81100597), the Natural Science Foundation Project of the Chongqing Science and Technology Commission (CSTC 2009BA5012), and the Natural Science Foundation of the Third Military Medical University (2012XJQ17, 2009XQN34).

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Zhou, J., Zhou, S. Inflammation: Therapeutic Targets for Diabetic Neuropathy. Mol Neurobiol 49, 536–546 (2014). https://doi.org/10.1007/s12035-013-8537-0

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