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Mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain

Osteoarthritis (OA) is the most common form of articular joint arthritis and a cause of significant morbidity. In this review, we present the role of nerve growth factor (NGF) in pain generation, relationship between NGF and OA pain, and pathogenic factors (interleukin-1β, transforming growth factor...

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Autores principales: Shang, Xiushuai, Wang, Zhaofei, Tao, Hairong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5546917/
https://www.ncbi.nlm.nih.gov/pubmed/28814877
http://dx.doi.org/10.2147/TCRM.S139814
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author Shang, Xiushuai
Wang, Zhaofei
Tao, Hairong
author_facet Shang, Xiushuai
Wang, Zhaofei
Tao, Hairong
author_sort Shang, Xiushuai
collection PubMed
description Osteoarthritis (OA) is the most common form of articular joint arthritis and a cause of significant morbidity. In this review, we present the role of nerve growth factor (NGF) in pain generation, relationship between NGF and OA pain, and pathogenic factors (interleukin-1β, transforming growth factor-β1, mechanical loading, and adipokines) involved in OA development. Since NGF blocking is an efficient way to inhibit OA-associated pain, we summarize four categories of drugs that target NGF/tropomyosin receptor kinase A (TrkA) signaling. In addition, we discuss the future of NGF/TrkA antagonists and underline their potential for use in OA pain relief. A better understanding of the causes and treatment of OA will facilitate the development of more effective methods of OA pain management.
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spelling pubmed-55469172017-08-16 Mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain Shang, Xiushuai Wang, Zhaofei Tao, Hairong Ther Clin Risk Manag Review Osteoarthritis (OA) is the most common form of articular joint arthritis and a cause of significant morbidity. In this review, we present the role of nerve growth factor (NGF) in pain generation, relationship between NGF and OA pain, and pathogenic factors (interleukin-1β, transforming growth factor-β1, mechanical loading, and adipokines) involved in OA development. Since NGF blocking is an efficient way to inhibit OA-associated pain, we summarize four categories of drugs that target NGF/tropomyosin receptor kinase A (TrkA) signaling. In addition, we discuss the future of NGF/TrkA antagonists and underline their potential for use in OA pain relief. A better understanding of the causes and treatment of OA will facilitate the development of more effective methods of OA pain management. Dove Medical Press 2017-08-01 /pmc/articles/PMC5546917/ /pubmed/28814877 http://dx.doi.org/10.2147/TCRM.S139814 Text en © 2017 Shang et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Review
Shang, Xiushuai
Wang, Zhaofei
Tao, Hairong
Mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain
title Mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain
title_full Mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain
title_fullStr Mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain
title_full_unstemmed Mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain
title_short Mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain
title_sort mechanism and therapeutic effectiveness of nerve growth factor in osteoarthritis pain
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5546917/
https://www.ncbi.nlm.nih.gov/pubmed/28814877
http://dx.doi.org/10.2147/TCRM.S139814
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