Progress on relationship between transforming growth factor-beta1 and tendinopathy.
10.3969/j.issn.1003-0034.2019.04.017
- Author:
Feng GAO
;
Chun-Bao LI
;
Jing-Bin ZHOU
;
Xue-Zhen SHEN
;
Bo HU
;
Ming LU
;
Yu-Feng LIU
;
Bai-Qing ZHANG
;
Ye-Han FANG
;
Yu-Jie LIU
1
,
2
Author Information
1. Department of Orthopaedics, Chinese PLA General Hospital, Beijing 100853, China
2. 13701356381@163.com.
- Publication Type:Journal Article
- Keywords:
Review literature;
Tendinopathy;
Transforming growth factor beta1
- MeSH:
Fibrosis;
Humans;
Signal Transduction;
Tendinopathy;
Transforming Growth Factor beta1
- From:
China Journal of Orthopaedics and Traumatology
2019;32(4):377-382
- CountryChina
- Language:Chinese
-
Abstract:
As a common soft tissue disease, the mechanism of tendinopathy has not been clarified and is lack of effective treatment method. Change of tissue fibrosis is the one of the main pathological features. Transforming growth factor beta 1 (TGF-β1), which is one of the important factor, participated in fibrosis. Inconsonant expressions of TGF-β1 could be found in tendinopathy. The studies are still controversial, but the vast majority of studies had showed that TGF-β1 was abnormal, and it is given priority to increase, which means that TGF-β1 plays an important role in the process of tendinopathy. In the process of tendon injuries and repairs, the time of TGF-β1 increasing is inconsistent. The time for TGF-β1 plays a significant role has not been determined. TGF-β1 has abnormal expressions in both tendinopathy and tendon repairs, which are two opposite processes. Thus, it may not be a one-way adjustment factor, but has a pleiotropic. Recent studies showed that TGF-β1 was considered as binding to receptor and transferring signal into the cell. Now there are three different receptors are found. The classical pathway of TGF-β1 in intracellular signal transduction is mainly through activation of Smad pathway. In the same time, there are also some non-classical pathways. TGF-β1 could break balance of extracellular matrix, which may be a reason to cause tendinopathy. But the regulations of TGF-β1 on the extracellular matrix are complex and diverse, further studies are required. Existing researches showed that the performance of treatments on tendinopathy is unsatisfied by blocking TGF-β1 downstream pathway. Therefore, it is a good way to study the upstream mechanism of produce TGF-β1. It may be an effective method to find new targets to inhibit the development of tendinopathy better by finding the original source of TGF-β1.
