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Curr Drug Targets. 2019 Sep 6. doi: 10.2174/1389450120666190906153652. [Epub ahead of print]

The Therapeutic Potential of Chemokines in the Treatment of Chemotherapy-Induced Peripheral Neuropathy.

Author information

1
State Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing 210009, PR. China.
2
Department of Pharmacy, Children`s Hospital of Nanjing Medical University, Nanjing 210008, P.R.. China.

Abstract

BACKGROUND:

One of the current challenges and complications of cancer therapy is chemotherapy-induced peripheral neuropathy (CIPN) and the neuropathic pain that is associated with this condition. Many major chemotherapeutic agents can cause neurotoxicity, significantly modulate the immune system and are always accompanied by various adverse effects. Recent evidence suggests that cross-talk occurs between the nervous system and the immune system during treatment with chemotherapeutic agents; thus, an emerging concept is that neuroinflammation is one of the major mechanisms underlying CIPN, as demonstrated by the upregulation of chemokines. Chemokines were originally identified as regulators of peripheral immune cell trafficking, and chemokines are also expressed on neurons and glial cells in the central nervous system (CNS).

OBJECTIVE:

In this review, we collect evidence demonstrating that chemokines are potential mediators and contributors to pain signalling in CIPN. The expression of chemokines and their receptors, such as CX3CL1/CX3CR1, CCL2/CCR2, CXCL1/CXCR2, CXCL12/CXCR4 and CCL3/CCR5, is altered in the pathological conditions of CIPN, and chemokine receptor antagonists attenuate neuropathic pain behaviour.

CONCLUSION:

By understanding the mechanisms of chemokine-mediated communication, we may reveal chemokine targets that can be used as novel therapeutic strategies for the treatment of CIPN.

KEYWORDS:

CCL2; CX3CL1; CXCL1; Chemokines; Chemotherapeutic agents; Chemotherapy-induced peripheral neuropathy; Neuroinflammation

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