TRPV4 Role in Neuropathic Pain Mechanisms in Rodents
Neuropathic pain is a chronic pain caused by a disease or damage to the somatosensory nervous system. The knowledge about the complete mechanisms is incomplete, but the role of oxidative compounds has been evaluated. In this context, we highlight the transient potential receptor vanilloid 4 (TRPV4),...
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2022-12-01
|
| Series: | Antioxidants |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2076-3921/12/1/24 |
| _version_ | 1797446914427322368 |
|---|---|
| author | Patrícia Rodrigues Náthaly Andrighetto Ruviaro Gabriela Trevisan |
| author_facet | Patrícia Rodrigues Náthaly Andrighetto Ruviaro Gabriela Trevisan |
| author_sort | Patrícia Rodrigues |
| collection | DOAJ |
| description | Neuropathic pain is a chronic pain caused by a disease or damage to the somatosensory nervous system. The knowledge about the complete mechanisms is incomplete, but the role of oxidative compounds has been evaluated. In this context, we highlight the transient potential receptor vanilloid 4 (TRPV4), a non-selective cation channel, that can be activated by oxidated compounds. In clinical trials, the TRPV4 antagonist (GSK2798745) has been well-tolerated in healthy volunteers. The TRPV4 activation by oxidative compounds, such as hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and nitric oxide (NO), has been researched in neuropathic pain models. Thus, the modulation of TRPV4 activation by decreasing oxidated compounds could represent a new pharmacological approach for neuropathic pain treatment. Most models evaluated the TRPV4 using knockout mice, antagonist or antisense treatments and detected mechanical allodynia, hyposmotic solution-induced nociception and heat hyperalgesia, but this channel is not involved in cold allodynia. Only H<sub>2</sub>O<sub>2</sub> and NO were evaluated as TRPV4 agonists, so one possible target to reduce neuropathic pain should focus on reducing these compounds. Therefore, this review outlines how the TRPV4 channel represents an innovative target to tackle neuropathic pain signaling in models induced by trauma, surgery, chemotherapy, cancer, diabetes and alcohol intake. |
| first_indexed | 2024-03-09T13:47:26Z |
| format | Article |
| id | doaj.art-b25dc7187c204b1fad9f58cc96a428a7 |
| institution | Directory Open Access Journal |
| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-09T13:47:26Z |
| publishDate | 2022-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj.art-b25dc7187c204b1fad9f58cc96a428a72023-11-30T20:57:16ZengMDPI AGAntioxidants2076-39212022-12-011212410.3390/antiox12010024TRPV4 Role in Neuropathic Pain Mechanisms in RodentsPatrícia Rodrigues0Náthaly Andrighetto Ruviaro1Gabriela Trevisan2Graduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Santa Maria 97105-900, RS, BrazilGraduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Santa Maria 97105-900, RS, BrazilGraduated Program in Pharmacology, Federal University of Santa Maria (UFSM), Santa Maria 97105-900, RS, BrazilNeuropathic pain is a chronic pain caused by a disease or damage to the somatosensory nervous system. The knowledge about the complete mechanisms is incomplete, but the role of oxidative compounds has been evaluated. In this context, we highlight the transient potential receptor vanilloid 4 (TRPV4), a non-selective cation channel, that can be activated by oxidated compounds. In clinical trials, the TRPV4 antagonist (GSK2798745) has been well-tolerated in healthy volunteers. The TRPV4 activation by oxidative compounds, such as hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and nitric oxide (NO), has been researched in neuropathic pain models. Thus, the modulation of TRPV4 activation by decreasing oxidated compounds could represent a new pharmacological approach for neuropathic pain treatment. Most models evaluated the TRPV4 using knockout mice, antagonist or antisense treatments and detected mechanical allodynia, hyposmotic solution-induced nociception and heat hyperalgesia, but this channel is not involved in cold allodynia. Only H<sub>2</sub>O<sub>2</sub> and NO were evaluated as TRPV4 agonists, so one possible target to reduce neuropathic pain should focus on reducing these compounds. Therefore, this review outlines how the TRPV4 channel represents an innovative target to tackle neuropathic pain signaling in models induced by trauma, surgery, chemotherapy, cancer, diabetes and alcohol intake.https://www.mdpi.com/2076-3921/12/1/24chronic painoxidative stressTRP channelsallodyniaTRPV1TRPA1 |
| spellingShingle | Patrícia Rodrigues Náthaly Andrighetto Ruviaro Gabriela Trevisan TRPV4 Role in Neuropathic Pain Mechanisms in Rodents Antioxidants chronic pain oxidative stress TRP channels allodynia TRPV1 TRPA1 |
| title | TRPV4 Role in Neuropathic Pain Mechanisms in Rodents |
| title_full | TRPV4 Role in Neuropathic Pain Mechanisms in Rodents |
| title_fullStr | TRPV4 Role in Neuropathic Pain Mechanisms in Rodents |
| title_full_unstemmed | TRPV4 Role in Neuropathic Pain Mechanisms in Rodents |
| title_short | TRPV4 Role in Neuropathic Pain Mechanisms in Rodents |
| title_sort | trpv4 role in neuropathic pain mechanisms in rodents |
| topic | chronic pain oxidative stress TRP channels allodynia TRPV1 TRPA1 |
| url | https://www.mdpi.com/2076-3921/12/1/24 |
| work_keys_str_mv | AT patriciarodrigues trpv4roleinneuropathicpainmechanismsinrodents AT nathalyandrighettoruviaro trpv4roleinneuropathicpainmechanismsinrodents AT gabrielatrevisan trpv4roleinneuropathicpainmechanismsinrodents |