Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain

被引:72
作者
Brandolini, Laura [1 ]
d'Angelo, Michele [2 ]
Antonosante, Andrea [2 ]
Cimini, Annamaria [2 ,3 ,4 ]
Allegretti, Marcello [1 ]
机构
[1] Dompe Farmaceutici SpA, Via Campo Pile, I-67100 Laquila, Italy
[2] Univ Aquila, Dept Life Hlth & Environm Sci, I-67100 Laquila, Italy
[3] Temple Univ, Sbarro Inst Canc Res & Mol Med, Philadelphia, PA 19122 USA
[4] Temple Univ, Ctr Biotechnol, Philadelphia, PA 19122 USA
关键词
chemotherapy; peripheral nervous system; central nervous system; inflammatory mediators; cytokines; chemokines; INDUCED PERIPHERAL NEUROPATHY; TUMOR-NECROSIS-FACTOR; DORSAL-ROOT GANGLION; PROINFLAMMATORY CYTOKINE EXPRESSION; MONOCYTE CHEMOATTRACTANT PROTEIN-1; BREAST-CANCER; MECHANICAL ALLODYNIA; SCHWANN-CELLS; GLIAL-CELLS; RAT MODEL;
D O I
10.3390/ijms20122904
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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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页数:13
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