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Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain

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 targ...

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Autores principales: Brandolini, Laura, d’Angelo, Michele, Antonosante, Andrea, Cimini, Annamaria, Allegretti, Marcello
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627296/
https://www.ncbi.nlm.nih.gov/pubmed/31197114
http://dx.doi.org/10.3390/ijms20122904
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author Brandolini, Laura
d’Angelo, Michele
Antonosante, Andrea
Cimini, Annamaria
Allegretti, Marcello
author_facet Brandolini, Laura
d’Angelo, Michele
Antonosante, Andrea
Cimini, Annamaria
Allegretti, Marcello
author_sort Brandolini, Laura
collection PubMed
description 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.
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spelling pubmed-66272962019-07-23 Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain Brandolini, Laura d’Angelo, Michele Antonosante, Andrea Cimini, Annamaria Allegretti, Marcello Int J Mol Sci Review 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. MDPI 2019-06-14 /pmc/articles/PMC6627296/ /pubmed/31197114 http://dx.doi.org/10.3390/ijms20122904 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Brandolini, Laura
d’Angelo, Michele
Antonosante, Andrea
Cimini, Annamaria
Allegretti, Marcello
Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain
title Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain
title_full Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain
title_fullStr Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain
title_full_unstemmed Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain
title_short Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain
title_sort chemokine signaling in chemotherapy-induced neuropathic pain
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627296/
https://www.ncbi.nlm.nih.gov/pubmed/31197114
http://dx.doi.org/10.3390/ijms20122904
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