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Mitochondrial dysfunction in the pathogenesis of chemotherapy-induced peripheral neuropathy

Research output: Chapter in Book/Report/Conference proceedingChapter

Original languageEnglish
Title of host publicationInternational Review of Neurobiology
Subtitle of host publicationMitochondrial Dysfunction in Neurodegeneration and Peripheral Neuropathies
EditorsPaul Fernyhough, Nigel A. Calcutt
PublisherElsevier
Chapter5
Pages83-126
Number of pages44
Volume145
ISBN (Print)978-0-12-817224-7
DOIs
Accepted/In press6 Jun 2019
Published20 Jun 2019

Publication series

NameInternational Review of Neurobiology
Volume145
ISSN (Print)0074-7742
ISSN (Electronic)2162-5514

King's Authors

Abstract

Several first-line chemotherapeutic agents, including taxanes, platinum agents and proteasome inhibitors, are associated with the dose-limiting side effect of chemotherapy-induced peripheral neuropathy (CIPN). CIPN predominantly manifests as sensory symptoms, which are likely due to drug accumulation within peripheral nervous tissues rather than the central nervous system. No treatment is currently available to prevent or reverse CIPN. The causal mechanisms underlying CIPN are not yet fully understood. Mitochondrial dysfunction has emerged as a major factor contributing to the development and maintenance of CIPN. This chapter will provide an overview of both clinical and preclinical data supporting this hypothesis. We will review the studies reporting the nature of mitochondrial dysfunction evoked by chemotherapy in terms of changes in mitochondrial morphology, bioenergetics and reactive oxygen species (ROS) generation. Furthermore, we will discuss the in vivo effects of pharmacological interventions that counteract chemotherapy-evoked mitochondrial dysfunction and ameliorate pain-like behaviour.

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