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Review
. 2019 Jun 14;20(12):2904.
doi: 10.3390/ijms20122904.

Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain

Laura Brandolini  1 , Michele d'Angelo  2 , Andrea Antonosante  3 , Marcello Allegretti  4   5 , Annamaria Cimini  6
Affiliations
Review

Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain

Laura Brandolini et al. Int J Mol Sci. .

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) is a side effect of chemotherapics such as taxanes, vinca alkaloids, and platinum compounds. In recent years, several reports have indicated the involvement of different molecular mechanisms in CIPN. The pathways described so far are diverse and target various components of the peripheral Nervous System (PNS). Among the contributors to neuropathic pain, inflammation has been indicated as a powerful driver of CIPN. Several pieces of evidence have demonstrated a chemotherapy-induced increase in peripheral pro-inflammatory cytokines and a strong correlation with peripheral neuropathy. At present, there are not adequate strategies to prevent CIPN, although there are drugs for treating CIPN, such as duloxetine, that have displayed a moderate effect on CIPN. In this review, we focus on the players involved in CIPN with a particular emphasis on chemokine signaling.

Keywords: central nervous system; chemokines; chemotherapy; cytokines; inflammatory mediators; peripheral nervous system.

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Conflict of interest statement

The Authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Summary scheme indicating the different players driving chemotherapy-induced peripheral neuropathy (CIPN).
See this image and copyright information in PMC

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