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Targeting neuroinflammation in neuropathic pain and opioid use
Neuropathic pain arises from injuries to the nervous system. It affects 20% of the adult US population and poses a major socioeconomic burden yet remains exceedingly difficult to treat. Current therapeutic approaches have limited efficacy and a large side effect profile that impedes their ability to...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Rockefeller University Press
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9793426/ https://www.ncbi.nlm.nih.gov/pubmed/36562735 http://dx.doi.org/10.1084/jem.20221244 |
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author | Salvemini, Daniela Doyle, Timothy M. |
author_facet | Salvemini, Daniela Doyle, Timothy M. |
author_sort | Salvemini, Daniela |
collection | PubMed |
description | Neuropathic pain arises from injuries to the nervous system. It affects 20% of the adult US population and poses a major socioeconomic burden yet remains exceedingly difficult to treat. Current therapeutic approaches have limited efficacy and a large side effect profile that impedes their ability to treat neuropathic pain effectively. Preclinical research over the last 30 yr has established the critical role that pro-inflammatory neuro–immune cell interactions have in the development and maintenance of neuropathic pain arising from various etiologies. Pro-inflammatory neuro–immune cell interactions also underlie the development of adverse side effects of opioids and the loss of their efficacy to treat pain. Evidence from work in our lab and others in preclinical animal models have shown that signaling from the bioactive sphingolipid, sphingosine-1-phosphate (S1P), through the S1P receptor subtype 1 (S1PR1) modulates neuro–immune cell interactions. Here, we discuss how targeting S1P/S1PR1 signaling with S1PR1 antagonists already Food and Drug Administration–approved or in clinical trials for multiple sclerosis can provide a viable pharmacotherapeutic approach to reduce neuro-immune cell inflammatory signaling and potentially treat patients suffering neuropathic pain and the adverse effects of opioids. |
format | Online Article Text |
id | pubmed-9793426 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-97934262023-06-23 Targeting neuroinflammation in neuropathic pain and opioid use Salvemini, Daniela Doyle, Timothy M. J Exp Med Viewpoint Neuropathic pain arises from injuries to the nervous system. It affects 20% of the adult US population and poses a major socioeconomic burden yet remains exceedingly difficult to treat. Current therapeutic approaches have limited efficacy and a large side effect profile that impedes their ability to treat neuropathic pain effectively. Preclinical research over the last 30 yr has established the critical role that pro-inflammatory neuro–immune cell interactions have in the development and maintenance of neuropathic pain arising from various etiologies. Pro-inflammatory neuro–immune cell interactions also underlie the development of adverse side effects of opioids and the loss of their efficacy to treat pain. Evidence from work in our lab and others in preclinical animal models have shown that signaling from the bioactive sphingolipid, sphingosine-1-phosphate (S1P), through the S1P receptor subtype 1 (S1PR1) modulates neuro–immune cell interactions. Here, we discuss how targeting S1P/S1PR1 signaling with S1PR1 antagonists already Food and Drug Administration–approved or in clinical trials for multiple sclerosis can provide a viable pharmacotherapeutic approach to reduce neuro-immune cell inflammatory signaling and potentially treat patients suffering neuropathic pain and the adverse effects of opioids. Rockefeller University Press 2022-12-23 /pmc/articles/PMC9793426/ /pubmed/36562735 http://dx.doi.org/10.1084/jem.20221244 Text en © 2022 Salvemini and Doyle https://creativecommons.org/licenses/by-nc-sa/4.0/http://www.rupress.org/terms/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Viewpoint Salvemini, Daniela Doyle, Timothy M. Targeting neuroinflammation in neuropathic pain and opioid use |
title | Targeting neuroinflammation in neuropathic pain and opioid use |
title_full | Targeting neuroinflammation in neuropathic pain and opioid use |
title_fullStr | Targeting neuroinflammation in neuropathic pain and opioid use |
title_full_unstemmed | Targeting neuroinflammation in neuropathic pain and opioid use |
title_short | Targeting neuroinflammation in neuropathic pain and opioid use |
title_sort | targeting neuroinflammation in neuropathic pain and opioid use |
topic | Viewpoint |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9793426/ https://www.ncbi.nlm.nih.gov/pubmed/36562735 http://dx.doi.org/10.1084/jem.20221244 |
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