Sodium Channels, Mitochondria, and Axonal Degeneration in Peripheral Neuropathy

Anna-Karin Persson, Janneke G. J. Hoeijmakers, Mark Estacion, Joel A. Black, Stephen G. Waxman*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Peripheral neuropathy results from damage to peripheral nerves and is often accompanied by pain in affected limbs. Treatment represents an unmet medical need and a thorough understanding of the mechanisms underlying axonal injury is needed. Longer nerve fibers tend to degenerate first (length-dependence), and patients carrying pathogenic mutations throughout life usually become symptomatic in mid- or late-life (time-dependence). The activity of voltage gated sodium channels can contribute to axonal injury and sodium channel gain-of-function mutations have been linked to peripheral neuropathy. Recent studies have implicated sodium channel activity, mitochondria(compromise, and reverse-mode Na+/Ca2+ exchange in time- and length-dependent axonal injury. Elucidation of molecular mechanisms underlying axonal injury in peripheral neuropathy may provide new therapeutic strategies for this painful and debilitating condition.
Original languageEnglish
Pages (from-to)377-390
JournalTrends in Molecular Medicine
Volume22
Issue number5
DOIs
Publication statusPublished - May 2016

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