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Chemotherapy-induced peripheral neuropathy: What do we know about mechanisms?

Abstract：

:Cisplatin, oxaliplatin, paclitaxel, vincristine and bortezomib are some of the most effective drugs successfully employed (alone or in combinations) as first-line treatment for common cancers. However they often caused severe peripheral neurotoxicity and neuropathic pain. Structural deficits in Dorsal Root Ganglia and sensory nerves caused symptoms as sensory loss, paresthesia, dysaesthesia and numbness that result in patient' suffering and also limit the life-saving therapy. Several scientists have explored the various mechanisms involved in the onset of chemotherapy-related peripheral neurotoxicity identifying molecular targets useful for the development of selected neuroprotective strategies. Dorsal Root Ganglia sensory neurons, satellite cells, Schwann cells, as well as neuronal and glial cells in the spinal cord, are the preferential sites in which chemotherapy neurotoxicity occurs. DNA damage, alterations in cellular system repairs, mitochondria changes, increased intracellular reactive oxygen species, alterations in ion channels, glutamate signalling, MAP-kinases and nociceptors ectopic activation are among the events that trigger the onset of peripheral neurotoxicity and neuropathic pain. In the present work we review the role of the main players in determining the pathogenesis of anticancer drugs-induced peripheral neuropathy.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Carozzi VA,Canta A,Chiorazzi A

doi

10.1016/j.neulet.2014.10.014

subject

Has Abstract

pub_date

2015-06-02 00:00:00

pages

90-107

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(14)00818-0

journal_volume

596

pub_type

杂志文章,评审

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