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Review ArticleReview Article

Diabetic Peripheral Neuropathy: Should a Chaperone Accompany Our Therapeutic Approach?

Kevin L. Farmer, Chengyuan Li and Rick T. Dobrowsky
Emily E. Scott, ASSOCIATE EDITOR
Pharmacological Reviews October 2012, 64 (4) 880-900; DOI: https://doi.org/10.1124/pr.111.005314
Kevin L. Farmer
Department of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas
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Chengyuan Li
Department of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas
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Rick T. Dobrowsky
Department of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas
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Emily E. Scott
Department of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas
Roles: ASSOCIATE EDITOR
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Abstract

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes that is associated with axonal atrophy, demyelination, blunted regenerative potential, and loss of peripheral nerve fibers. The development and progression of DPN is due in large part to hyperglycemia but is also affected by insulin deficiency and dyslipidemia. Although numerous biochemical mechanisms contribute to DPN, increased oxidative/nitrosative stress and mitochondrial dysfunction seem intimately associated with nerve dysfunction and diminished regenerative capacity. Despite advances in understanding the etiology of DPN, few approved therapies exist for the pharmacological management of painful or insensate DPN. Therefore, identifying novel therapeutic strategies remains paramount. Because DPN does not develop with either temporal or biochemical uniformity, its therapeutic management may benefit from a multifaceted approach that inhibits pathogenic mechanisms, manages inflammation, and increases cytoprotective responses. Finally, exercise has long been recognized as a part of the therapeutic management of diabetes, and exercise can delay and/or prevent the development of painful DPN. This review presents an overview of existing therapies that target both causal and symptomatic features of DPN and discusses the role of up-regulating cytoprotective pathways via modulating molecular chaperones. Overall, it may be unrealistic to expect that a single pharmacologic entity will suffice to ameliorate the multiple symptoms of human DPN. Thus, combinatorial therapies that target causal mechanisms and enhance endogenous reparative capacity may enhance nerve function and improve regeneration in DPN if they converge to decrease oxidative stress, improve mitochondrial bioenergetics, and increase response to trophic factors.

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  • This article is available online at http://pharmrev.aspetjournals.org.

    http://dx.doi.org/10.1124/pr.111.005314.

  • © 2012 by The American Society for Pharmacology and Experimental Therapeutics
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Pharmacological Reviews: 64 (4)
Pharmacological Reviews
Vol. 64, Issue 4
1 Oct 2012
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Review ArticleReview Article

MECHANISMS AND THERAPIES IN DIABETIC PERIPHERAL NEUROPATHY

Kevin L. Farmer, Chengyuan Li and Rick T. Dobrowsky
Pharmacological Reviews October 1, 2012, 64 (4) 880-900; DOI: https://doi.org/10.1124/pr.111.005314

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Review ArticleReview Article

MECHANISMS AND THERAPIES IN DIABETIC PERIPHERAL NEUROPATHY

Kevin L. Farmer, Chengyuan Li and Rick T. Dobrowsky
Pharmacological Reviews October 1, 2012, 64 (4) 880-900; DOI: https://doi.org/10.1124/pr.111.005314
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    • Abstract
    • I. Introduction
    • II. Pathogenesis of Diabetic Peripheral Neuropathy
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