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TGF-β signaling and the development of osteoarthritis
Osteoarthritis (OA) is a common joint degenerative disease affecting the whole joint structure, including articular cartilage, subchondral bone and synovial tissue. Although extensive work has been done in recent years to explore the molecular mechanism underlying this disease, the pathogenesis of O...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4274935/ https://www.ncbi.nlm.nih.gov/pubmed/25541594 http://dx.doi.org/10.1038/boneres.2014.2 |
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author | Shen, Jie Li, Shan Chen, Di |
author_facet | Shen, Jie Li, Shan Chen, Di |
author_sort | Shen, Jie |
collection | PubMed |
description | Osteoarthritis (OA) is a common joint degenerative disease affecting the whole joint structure, including articular cartilage, subchondral bone and synovial tissue. Although extensive work has been done in recent years to explore the molecular mechanism underlying this disease, the pathogenesis of OA is still poorly understood and currently, there is no effective disease-modifying treatment for OA. Recently, both in vitro and in vivo studies suggest that confirmed (TGF-β)/SMAD pathway plays a critical role during OA development. This short review will focus on the function and signaling mechanisms of TGF-β/SMAD pathway in articular chondrocytes, mesenchymal progenitor cells of subchondral bone and synovial lining cells during OA development. |
format | Online Article Text |
id | pubmed-4274935 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-42749352014-12-23 TGF-β signaling and the development of osteoarthritis Shen, Jie Li, Shan Chen, Di Bone Res Review Article Osteoarthritis (OA) is a common joint degenerative disease affecting the whole joint structure, including articular cartilage, subchondral bone and synovial tissue. Although extensive work has been done in recent years to explore the molecular mechanism underlying this disease, the pathogenesis of OA is still poorly understood and currently, there is no effective disease-modifying treatment for OA. Recently, both in vitro and in vivo studies suggest that confirmed (TGF-β)/SMAD pathway plays a critical role during OA development. This short review will focus on the function and signaling mechanisms of TGF-β/SMAD pathway in articular chondrocytes, mesenchymal progenitor cells of subchondral bone and synovial lining cells during OA development. Nature Publishing Group 2014-05-27 /pmc/articles/PMC4274935/ /pubmed/25541594 http://dx.doi.org/10.1038/boneres.2014.2 Text en Copyright © 2014 Sichuan University. http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/ |
spellingShingle | Review Article Shen, Jie Li, Shan Chen, Di TGF-β signaling and the development of osteoarthritis |
title | TGF-β signaling and the development of osteoarthritis |
title_full | TGF-β signaling and the development of osteoarthritis |
title_fullStr | TGF-β signaling and the development of osteoarthritis |
title_full_unstemmed | TGF-β signaling and the development of osteoarthritis |
title_short | TGF-β signaling and the development of osteoarthritis |
title_sort | tgf-β signaling and the development of osteoarthritis |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4274935/ https://www.ncbi.nlm.nih.gov/pubmed/25541594 http://dx.doi.org/10.1038/boneres.2014.2 |
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