TRPV receptors in pain research: Bridging molecular mechanisms to clinical treatments

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Abstract

Objective The cation channels known as transient receptor potential vanilloid (TRPV) are shown in various groups of tissues, such as the heart, lung, and brain, and in both excitable and non-excitable cells. Numerous isoforms of the TRPV channel family are triggered by various chemical and physical stimuli. It has recently been demonstrated that reactive oxygen species can also directly or indirectly activate TRPV channels. Neurodegenerative disorders (NDs) like Parkinson's and Alzheimer's disease are largely caused by oxidative stress, and TRPV channels play a role in the development of these diseases through the mechanisms involving altered crosstalk between oxidative stress, Ca2+ regulation, and the generation of inflammatory mediators. Additionally, it has been noted that pain is a complicated problem for people with Parkinson's and Alzheimer's illnesses, and there is ongoing debate on how best to manage pain in those patients. Methods Various search databases were used with proper inclusion and exclusion criteria, like inclusion criteria: TRPV channels, NDs, neuropathic pain, and including unpleasant stimuli, temperature, pH, and osmotic pressure. Results TRPV has been studied as a possible target for treating NDs and pain management. TRPV channels have been shown in various NDs to have elevated activity, which has led to recent research highlighting their potential as therapeutic targets for NDs. In preclinical models of NDs, it has been demonstrated that altering TRPV channel activity has neuroprotective effects and enhances cognitive performance. Conclusion This review discusses the potential role of TRPV channels in pain related to NDs and examines their feasibility as pharmaceutical targets for managing pain in affected patients.

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APA

Bana, S., Sartaj, A., Goel, R., Usmani, J., Ansari, M. N., & Gupta, A. K. (2025). TRPV receptors in pain research: Bridging molecular mechanisms to clinical treatments. Letters in Drug Design and Discovery, 22(10). https://doi.org/10.1016/j.lddd.2025.100064

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