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Mediators of Inflammation - Volume 2017 2017, Article ID 9383184, 8 pages - https:-doi.org-10.1155-2017-9383184

Review Article

Pain Research Center, Department of Anesthesiology, University of Cincinnati Medical Center, Cincinnati, OH, USA

Department of Physiology, College of Medicine, Gachon University, Incheon 21999, Republic of Korea

Correspondence should be addressed to Temugin Berta and Chul-Kyu Park

Received 18 August 2016; Accepted 6 November 2016; Published 7 February 2017

Academic Editor: Liliana Bernardino

Copyright © 2017 Temugin Berta et al. 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.

Abstract

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.





Author: Temugin Berta, Jee Eun Lee, and Chul-Kyu Park

Source: https://www.hindawi.com/



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