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Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A review

The degeneration of articular cartilage tissue is the most common cause of articular cartilage diseases such as osteoarthritis. There are limitations in chondrocyte self-renewal and conventional treatments. During cartilage regeneration and repair, growth factors are typically used to induce cartila...

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Detalles Bibliográficos
Autores principales: Niu, Jing, Liu, Yanli, Wang, Junjun, Wang, Hui, Zhao, Ying, Zhang, Min
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10145989/
https://www.ncbi.nlm.nih.gov/pubmed/37115081
http://dx.doi.org/10.1097/MD.0000000000033651
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author Niu, Jing
Liu, Yanli
Wang, Junjun
Wang, Hui
Zhao, Ying
Zhang, Min
author_facet Niu, Jing
Liu, Yanli
Wang, Junjun
Wang, Hui
Zhao, Ying
Zhang, Min
author_sort Niu, Jing
collection PubMed
description The degeneration of articular cartilage tissue is the most common cause of articular cartilage diseases such as osteoarthritis. There are limitations in chondrocyte self-renewal and conventional treatments. During cartilage regeneration and repair, growth factors are typically used to induce cartilage differentiation in stem cells. The role of thrombospondin-2 in cartilage formation has received much attention in recent years. This paper reviews the role of thrombospondin-2 in cartilage regeneration and the important role it plays in protecting cartilage from damage caused by inflammation or trauma and in the regenerative repair of cartilage by binding to different receptors and activating different intracellular signaling pathways. These studies provide new ideas for cartilage repair in clinical settings.
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spelling pubmed-101459892023-04-29 Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A review Niu, Jing Liu, Yanli Wang, Junjun Wang, Hui Zhao, Ying Zhang, Min Medicine (Baltimore) 6300 The degeneration of articular cartilage tissue is the most common cause of articular cartilage diseases such as osteoarthritis. There are limitations in chondrocyte self-renewal and conventional treatments. During cartilage regeneration and repair, growth factors are typically used to induce cartilage differentiation in stem cells. The role of thrombospondin-2 in cartilage formation has received much attention in recent years. This paper reviews the role of thrombospondin-2 in cartilage regeneration and the important role it plays in protecting cartilage from damage caused by inflammation or trauma and in the regenerative repair of cartilage by binding to different receptors and activating different intracellular signaling pathways. These studies provide new ideas for cartilage repair in clinical settings. Lippincott Williams & Wilkins 2023-04-25 /pmc/articles/PMC10145989/ /pubmed/37115081 http://dx.doi.org/10.1097/MD.0000000000033651 Text en Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY) (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle 6300
Niu, Jing
Liu, Yanli
Wang, Junjun
Wang, Hui
Zhao, Ying
Zhang, Min
Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A review
title Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A review
title_full Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A review
title_fullStr Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A review
title_full_unstemmed Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A review
title_short Thrombospondin-2 acts as a critical regulator of cartilage regeneration: A review
title_sort thrombospondin-2 acts as a critical regulator of cartilage regeneration: a review
topic 6300
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10145989/
https://www.ncbi.nlm.nih.gov/pubmed/37115081
http://dx.doi.org/10.1097/MD.0000000000033651
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