HDAC inhibitors as a potential therapy for chemotherapy-induced neuropathic pain
- PMID: 38761314
- DOI: 10.1007/s10787-024-01488-x
HDAC inhibitors as a potential therapy for chemotherapy-induced neuropathic pain
Abstract
Cancer, a chronic disease characterized by uncontrolled cell development, kills millions of people globally. The WHO reported over 10 million cancer deaths in 2020. Anticancer medications destroy healthy and malignant cells. Cancer treatment induces neuropathy. Anticancer drugs cause harm to spinal cord, brain, and peripheral nerve somatosensory neurons, causing chemotherapy-induced neuropathic pain. The chemotherapy-induced mechanisms underlying neuropathic pain are not fully understood. However, neuroinflammation has been identified as one of the various pathways associated with the onset of chemotherapy-induced neuropathic pain. The neuroinflammatory processes may exhibit varying characteristics based on the specific type of anticancer treatment delivered. Neuroinflammatory characteristics have been observed in the spinal cord, where microglia and astrocytes have a significant impact on the development of chemotherapy-induced peripheral neuropathy. The patient's quality of life might be affected by sensory deprivation, loss of consciousness, paralysis, and severe disability. High cancer rates and ineffective treatments are associated with this disease. Recently, histone deacetylases have become a novel treatment target for chemotherapy-induced neuropathic pain. Chemotherapy-induced neuropathic pain may be treated with histone deacetylase inhibitors. Histone deacetylase inhibitors may be a promising therapeutic treatment for chemotherapy-induced neuropathic pain. Common chemotherapeutic drugs, mechanisms, therapeutic treatments for neuropathic pain, and histone deacetylase and its inhibitors in chemotherapy-induced neuropathic pain are covered in this paper. We propose that histone deacetylase inhibitors may treat several aspects of chemotherapy-induced neuropathic pain, and identifying these inhibitors as potentially unique treatments is crucial to the development of various chemotherapeutic combination treatments.
Keywords: Chemotherapy; Epigenetics; HDAC; HDAC inhibitor; Inflammation; Neuropathic pain.
© 2024. The Author(s), under exclusive licence to Springer Nature Switzerland AG.
Similar articles
-
Histone deacetylase as emerging pharmacological therapeutic target for neuropathic pain: From epigenetic to selective drugs.CNS Neurosci Ther. 2024 May;30(5):e14745. doi: 10.1111/cns.14745. CNS Neurosci Ther. 2024. PMID: 38715326 Free PMC article. Review.
-
Dual HDAC/BRD4 Inhibitors Relieves Neuropathic Pain by Attenuating Inflammatory Response in Microglia After Spared Nerve Injury.Neurotherapeutics. 2022 Sep;19(5):1634-1648. doi: 10.1007/s13311-022-01243-6. Epub 2022 May 2. Neurotherapeutics. 2022. PMID: 35501470 Free PMC article.
-
Combined inhibition of histone deacetylases and BET family proteins as epigenetic therapy for nerve injury-induced neuropathic pain.Pharmacol Res. 2021 Mar;165:105431. doi: 10.1016/j.phrs.2021.105431. Epub 2021 Jan 30. Pharmacol Res. 2021. PMID: 33529752
-
Dual BET/HDAC inhibition to relieve neuropathic pain: Recent advances, perspectives, and future opportunities.Pharmacol Res. 2021 Nov;173:105901. doi: 10.1016/j.phrs.2021.105901. Epub 2021 Sep 20. Pharmacol Res. 2021. PMID: 34547384
-
Neuroinflammatory Process Involved in Different Preclinical Models of Chemotherapy-Induced Peripheral Neuropathy.Front Immunol. 2021 Feb 4;11:626687. doi: 10.3389/fimmu.2020.626687. eCollection 2020. Front Immunol. 2021. PMID: 33613570 Free PMC article. Review.
Cited by
-
Exploring the Analgesic Potential of L-Lysine: Molecular Mechanisms, Preclinical Evidence, and Implications for Pharmaceutical Pain Therapy.Pharmaceutics. 2025 May 19;17(5):666. doi: 10.3390/pharmaceutics17050666. Pharmaceutics. 2025. PMID: 40430956 Free PMC article. Review.
-
Epigenetics-targeted drugs: current paradigms and future challenges.Signal Transduct Target Ther. 2024 Nov 26;9(1):332. doi: 10.1038/s41392-024-02039-0. Signal Transduct Target Ther. 2024. PMID: 39592582 Free PMC article. Review.
-
Emerging targets and translational challenges in treating paclitaxel-induced peripheral neuropathy.Mol Biol Rep. 2025 Aug 18;52(1):833. doi: 10.1007/s11033-025-10938-w. Mol Biol Rep. 2025. PMID: 40824316 Review.
References
-
- Abbadie C, Lindia JA, Cumiskey AM et al (2003) Impaired neuropathic pain responses in mice lacking the chemokine receptor CCR2. Proc Natl Acad Sci U S A 100(13):7947–7952. https://doi.org/10.1073/pnas.1331358100 - DOI - PubMed - PMC
-
- Akopian AN, Sivilotti L, Wood JN (1996) A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons. Nature 379(6562):257–262. https://doi.org/10.1038/379257a0 - DOI - PubMed
-
- Akopian AN, Souslova V, England S et al (1999) The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways. Nat Neurosci 2(6):541–548. https://doi.org/10.1038/9195 - DOI - PubMed
-
- Aley KO, Reichling DB, Levine JD (1996) Vincristine hyperalgesia in the rat: a model of painful vincristine neuropathy in humans. Neuroscience 73(1):259–265. https://doi.org/10.1016/0306-4522(96)00020-6 - DOI - PubMed
-
- Areti A, Yerra VG, Naidu V, Kumar A (2014) Oxidative stress and nerve damage: role in chemotherapy induced peripheral neuropathy. Redox Biol 2:289–295. https://doi.org/10.1016/j.redox.2014.01.006 - DOI - PubMed - PMC