Channelopathies, painful neuropathy, and diabetes: which way does the causal arrow point?

Janneke G. J. Hoeijmakers, Catharina G. Faber, Ingemar S. J. Merkies, Stephen G. Waxman*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

27 Citations (Web of Science)

Abstract

Diabetes mellitus, a major global health problem, is commonly associated with painful peripheral neuropathy, which can substantially erode quality of life. Despite its clinical importance, the pathophysiology of painful diabetic neuropathy is incompletely understood. It has traditionally been thought that diabetes may cause neuropathy in patients with appropriate genetic makeup. Here, we propose a hypothesis whereby painful neuropathy is not a complication of diabetes, but rather occurs as a result of mutations that, in parallel, confer vulnerability to injury in pancreatic beta cells and pain-signaling dorsal root ganglion (DRG) neurons. We suggest that mutations of sodium channel Na(V)1.7, which is present in both cell types, may increase susceptibility for development of diabetes via beta cell injury and produce painful neuropathy via a distinct effect on DRG neurons.
Original languageEnglish
Pages (from-to)544-550
JournalTrends in Molecular Medicine
Volume20
Issue number10
DOIs
Publication statusPublished - Oct 2014

Keywords

  • diabetes mellitus
  • diabetic neuropathy
  • painful neuropathy
  • sodium channelopathy
  • Ne(V)1.7
  • beta cells

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