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转化生长因子-β2在软骨发育及疾病中的作用。

The role of TGF-β2 in cartilage development and diseases.

作者信息

Duan Mengmeng, Wang Qingxuan, Liu Yang, Xie Jing

机构信息

State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

出版信息

Bone Joint Res. 2021 Aug;10(8):474-487. doi: 10.1302/2046-3758.108.BJR-2021-0086.

DOI:10.1302/2046-3758.108.BJR-2021-0086
PMID:34340528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8412840/
Abstract

Transforming growth factor-beta2 (TGF-β2) is recognized as a versatile cytokine that plays a vital role in regulation of joint development, homeostasis, and diseases, but its role as a biological mechanism is understood far less than that of its counterpart, TGF-β1. Cartilage as a load-resisting structure in vertebrates however displays a fragile performance when any tissue disturbance occurs, due to its lack of blood vessels, nerves, and lymphatics. Recent reports have indicated that TGF-β2 is involved in the physiological processes of chondrocytes such as proliferation, differentiation, migration, and apoptosis, and the pathological progress of cartilage such as osteoarthritis (OA) and rheumatoid arthritis (RA). TGF-β2 also shows its potent capacity in the repair of cartilage defects by recruiting autologous mesenchymal stem cells and promoting secretion of other growth factor clusters. In addition, some pioneering studies have already considered it as a potential target in the treatment of OA and RA. This article aims to summarize the current progress of TGF-β2 in cartilage development and diseases, which might provide new cues for remodelling of cartilage defect and intervention of cartilage diseases.

摘要

转化生长因子-β2(TGF-β2)是一种多功能细胞因子,在关节发育、稳态和疾病调控中发挥着至关重要的作用,但其作为一种生物学机制的作用远不如其对应物TGF-β1被了解得透彻。然而,软骨作为脊椎动物的承重结构,由于缺乏血管、神经和淋巴管,在发生任何组织紊乱时都表现出脆弱的性能。最近的报道表明,TGF-β2参与软骨细胞的增殖、分化、迁移和凋亡等生理过程,以及骨关节炎(OA)和类风湿关节炎(RA)等软骨的病理进展。TGF-β2还通过招募自体间充质干细胞和促进其他生长因子簇的分泌,在软骨缺损修复中显示出强大的能力。此外,一些开创性的研究已经将其视为OA和RA治疗的潜在靶点。本文旨在总结TGF-β2在软骨发育和疾病方面的当前进展,这可能为软骨缺损重塑和软骨疾病干预提供新的线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/84963685dee9/BJR-10-474-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/151000716b59/BJR-10-474-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/97a0e7935311/BJR-10-474-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/852bfc34c791/BJR-10-474-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/84963685dee9/BJR-10-474-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/151000716b59/BJR-10-474-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/f1ccf3718a5a/BJR-10-474-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/97a0e7935311/BJR-10-474-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/852bfc34c791/BJR-10-474-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cde/8412840/84963685dee9/BJR-10-474-g0005.jpg

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