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REVIEW article

Front. Mol. Neurosci.
Sec. Pain Mechanisms and Modulators
Volume 17 - 2024 | doi: 10.3389/fnmol.2024.1400118
This article is part of the Research Topic Molecular Mechanism of Neuroimmune Modulation and Synaptic Plasticity in Acute and Chronic Pain Volume II View all 4 articles

The Dual Role of TRPV1 in Peripheral Neuropathic Pain: Pain Switches Caused by its Sensitization or Desensitization

Provisionally accepted
Ning Gao Ning Gao *Meng Li Meng Li Weiming Wang Weiming Wang Zhen Liu Zhen Liu Yufeng Guo Yufeng Guo
  • Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China

The final, formatted version of the article will be published soon.

    The transient receptor potential vanilloid 1 (TRPV1) channel plays a dual role in peripheral neuropathic pain (NeuP) by acting as a "pain switch" through its sensitization and desensitization. Hyperalgesia, commonly resulting from tissue injury or inflammation, involves the sensitization of TRPV1 channels, which modulates sensory transmission from primary afferent nociceptors to spinal dorsal horn neurons.In chemotherapy-induced peripheral neuropathy (CIPN), TRPV1 is implicated in neuropathic pain mechanisms due to its interaction with ion channels, neurotransmitter signaling, and oxidative stress. Sensitization of TRPV1 in dorsal root ganglion neurons contributes to CIPN development, and inhibition of TRPV1 channels can reduce chemotherapy-induced mechanical hypersensitivity. In diabetic peripheral neuropathy (DPN), TRPV1 is involved in pain modulation through pathways including reactive oxygen species and cytokine production. TRPV1's interaction with TRPA1 channels further influences chronic pain onset and progression. Therapeutically, capsaicin, a TRPV1 agonist, can induce analgesia through receptor desensitization, while TRPV1 antagonists and siRNA targeting TRPV1 show promise in preclinical studies. Cannabinoid modulation of TRPV1 provides another potential pathway for alleviating neuropathic pain. This review summarizes recent preclinical research on TRPV1 in association with peripheral NeuP.

    Keywords: TRPV1, Peripheral neuropathic pain, Molecular mechanisms, sensitization, Desensitization

    Received: 13 Mar 2024; Accepted: 12 Aug 2024.

    Copyright: © 2024 Gao, Li, Wang, Liu and Guo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Ning Gao, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.