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Targeting glia for bone cancer pain
Ya-Qun Zhou1,2, Zheng Liu3, Hui-Quan Liu4
1a Research Center for Anesthesiology and Pain Medicine, Tongji Hospital, Tongji Medical College , Huazhong University of Science and Technology , Wuhan , China.
Introduction:
Bone cancer pain (BCP) remains to be a clinical challenge with limited pharmaceutical interventions. Therefore, novel therapeutic targets for the management of BCP are in desperate need. Recently, a growing body of evidence has suggested that glial cells may play a pivotal role in the pathogenesis of BCP. Areas covered: This review summarizes the recent progress in the understanding of glia in BCP and reveals the potential therapeutic targets in glia for BCP treatment. Expert opinion: Pharmacological interventions inhibiting the activation of glial cells, suppressing glia-derived proinflammatory cytokines, cell surface receptors, and the intracellular signaling pathways may be beneficial for the pain management of advanced cancer patients. However, these pharmacological interventions should not disrupt the normal function of glia cells since they play a vital supportive and protective role in the central nervous system.
Insights
Glial cells are key players in bone cancer pain (BCP). Targeting glial cell activation and their inflammatory products offers new therapeutic strategies for managing BCP.
Area of Science:
- Neuroscience
- Oncology
- Pain Management
Background:
- Bone cancer pain (BCP) presents a significant clinical challenge with limited effective pharmaceutical treatments.
- Emerging research highlights the crucial role of glial cells in the development and progression of BCP.
Purpose of the Study:
- To review current understanding of glial cell involvement in BCP.
- To identify potential therapeutic targets within glial cells for BCP management.
Main Methods:
- Literature review of recent scientific progress on glia in BCP.
- Analysis of studies investigating glial cell activation and signaling pathways in BCP.
Main Results:
- Glial cells significantly contribute to the pathogenesis of BCP.
- Inhibiting glial cell activation and suppressing glia-derived inflammatory mediators shows promise for BCP treatment.
Conclusions:
- Targeting glial cells, including their activation, proinflammatory cytokines, cell surface receptors, and intracellular signaling, may effectively manage BCP.
- Therapeutic strategies must preserve the essential supportive and protective functions of glia in the central nervous system.
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