Abstract |
Transforming growth factor-β(TGF-β) plays an important but diverse role in tendon injuries, such as collagen synthesis, cell proliferation, cell differentiation, and cell adhesion, leading to tendon healing and tendon fibrosis. In the well-known canonical TGF-β signalling pathway, TGF-β activates Smad signalling through its two cell surface receptors, which leads to Smad-mediated transcriptional regulation and is also regulated by inhibitory Smads, forming a negative feedback regulatory pathway. In the context of the canonical TGF-β signalling mechanism mediated by Smad, the activated receptors also send signals through other signal transducers, which in the backdrop of TGF-β signaling are collectively known as non-Smad signalling pathways. Activated TGF-β binds to the receptor and acts through these signalling pathways. Understanding the mechanism of the TGF-β signalling pathway and its role in tendon repair is of great significance for targeting the TGF-β signalling pathway to accelerate tendon healing and reduce tendon fibrosis.
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Authors | Yujie Li, Xinyue Liu, Xueli Liu, Yuanqiu Peng, Bin Zhu, Sheng Guo, Chenglong Wang, Dingxuan Wang, Sen Li |
Journal | Growth factors (Chur, Switzerland)
(Growth Factors)
Vol. 40
Issue 3-4
Pg. 98-107
(08 2022)
ISSN: 1029-2292 [Electronic] England |
PMID | 35707986
(Publication Type: Journal Article, Review)
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Chemical References |
- Smad Proteins
- Transforming Growth Factor beta
- Transforming Growth Factor beta1
- Transforming Growth Factors
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Topics |
- Fibrosis
- Humans
- Signal Transduction
(physiology)
- Smad Proteins
(metabolism)
- Tendons
(metabolism)
- Transforming Growth Factor beta
(metabolism)
- Transforming Growth Factor beta1
- Transforming Growth Factors
(metabolism)
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