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Unconventional Role of Caspase-6 in Spinal Microglia Activation and Chronic Pain

Chronic pain affects ~20% of the worldwide population. The clinical management of chronic pain is mostly palliative and results in limited success. Current treatments mostly target the symptoms or neuronal signaling of chronic pain. It has been increasingly recognized that glial cells, such as micro...

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Detalles Bibliográficos
Autores principales: Berta, Temugin, Lee, Jee Eun, Park, Chul-Kyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5320069/
https://www.ncbi.nlm.nih.gov/pubmed/28270702
http://dx.doi.org/10.1155/2017/9383184
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author Berta, Temugin
Lee, Jee Eun
Park, Chul-Kyu
author_facet Berta, Temugin
Lee, Jee Eun
Park, Chul-Kyu
author_sort Berta, Temugin
collection PubMed
description Chronic pain affects ~20% of the worldwide population. The clinical management of chronic pain is mostly palliative and results in limited success. Current treatments mostly target the symptoms or neuronal signaling of chronic pain. It has been increasingly recognized that glial cells, such as microglia, and inflammatory signaling play a major role in the pathogenesis of chronic pain. Caspases (CASPs) are a family of protease enzymes involved in apoptosis and inflammation. They are pivotal components in a variety of neurological diseases. However, little is known about the role of CASPs in microglial modulation as to chronic pain. In particular, our recent studies have shown that CASP6 regulates chronic pain via microglial inflammatory signaling. Inhibition of microglia and CASP signaling might provide a new strategy for the prevention and treatment of chronic pain.
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spelling pubmed-53200692017-03-07 Unconventional Role of Caspase-6 in Spinal Microglia Activation and Chronic Pain Berta, Temugin Lee, Jee Eun Park, Chul-Kyu Mediators Inflamm Review Article Chronic pain affects ~20% of the worldwide population. The clinical management of chronic pain is mostly palliative and results in limited success. Current treatments mostly target the symptoms or neuronal signaling of chronic pain. It has been increasingly recognized that glial cells, such as microglia, and inflammatory signaling play a major role in the pathogenesis of chronic pain. Caspases (CASPs) are a family of protease enzymes involved in apoptosis and inflammation. They are pivotal components in a variety of neurological diseases. However, little is known about the role of CASPs in microglial modulation as to chronic pain. In particular, our recent studies have shown that CASP6 regulates chronic pain via microglial inflammatory signaling. Inhibition of microglia and CASP signaling might provide a new strategy for the prevention and treatment of chronic pain. Hindawi Publishing Corporation 2017 2017-02-07 /pmc/articles/PMC5320069/ /pubmed/28270702 http://dx.doi.org/10.1155/2017/9383184 Text en Copyright © 2017 Temugin Berta et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Berta, Temugin
Lee, Jee Eun
Park, Chul-Kyu
Unconventional Role of Caspase-6 in Spinal Microglia Activation and Chronic Pain
title Unconventional Role of Caspase-6 in Spinal Microglia Activation and Chronic Pain
title_full Unconventional Role of Caspase-6 in Spinal Microglia Activation and Chronic Pain
title_fullStr Unconventional Role of Caspase-6 in Spinal Microglia Activation and Chronic Pain
title_full_unstemmed Unconventional Role of Caspase-6 in Spinal Microglia Activation and Chronic Pain
title_short Unconventional Role of Caspase-6 in Spinal Microglia Activation and Chronic Pain
title_sort unconventional role of caspase-6 in spinal microglia activation and chronic pain
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5320069/
https://www.ncbi.nlm.nih.gov/pubmed/28270702
http://dx.doi.org/10.1155/2017/9383184
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