| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2794448 | Cytokine | 2012 | 7 Pages |
Chemotherapy-induced peripheral neuropathy (CIPN), a dose-limiting neurotoxic effect of chemotherapy, is the most common reason for early cessation of cancer treatment. This can result in an increased risk of recurrence and decreased survival rate. Inflammatory cascade activation, proinflammatory cytokine upregulation, and neuro-immune communication pathways play essential roles in the initiation and progression of CIPN. Most notably, TNF-α, IL-1β, IL-6, and CCL2 are involved in neuropathic pain. Further elucidation of the role of these cytokines could lead to their development and use as biomarkers for predicting the onset of painful peripheral neuropathy and early axonal damage. In this review, we provide evidence for the involvement of cytokines in CIPN, the possible underlying mechanisms, and their use as potential therapeutic targets and biomarkers to prevent and improve the painful peripheral neuropathy related to chemotherapeutic agents.
► CIPN is one of the most common reasons for early cessation of cancer treatment. ► Challenge: unknown underlying mechanism; unavailable prevention and treatment. ► Cytokines plays an essential role in the initiation and progression of painful CIPN. ► This review provides the possible mechanisms underlying painful CIPN. ► The possible therapeutic targets and biomarkers to prevent and improve painful CIPN.
