ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022
Inhibition of Integrin αvβ6 Activation of TGF-β Attenuates Tendinopathy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Hyperlipidemia-induced metabolic dysregulation impairs tendon homeostasis: the role of TGF-Frontiers in medicine · 2026Article
- Ectopic engraftment of nociceptive neurons derived from hPSCs for pain relief and joint homeostasis.bioRxiv : the preprint server for biology · 2025Article
- CTHRC1 Attenuates Tendinopathy via Enhancing EGFR/MAPK Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Myeloid Cells and Sensory Nerves Mediate Peritendinous Adhesion Formation via Prostaglandin E2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Cross-Talk between the TGF-β and Cell Adhesion Signaling Pathways in Cancer.International journal of medical sciences · 2024Review
- Whole Genome Expression Profiling of Semitendinosus Tendons from Children with Diplegic and Tetraplegic Cerebral Palsy.Biomedicines · 2023Article
- The Contribution of the Nrf2/ARE System to Mechanotransduction in Musculoskeletal and Periodontal Tissues.International journal of molecular sciences · 2023Review
- Mouse Achilles tendons exhibit collagen disorganization but minimal collagen denaturation during cyclic loading to failure.Journal of biomechanics · 2023Article
- Review of Basic Research about Ossification of the Spinal Ligaments Focusing on Animal Models.Journal of clinical medicine · 2023Review
- CD200 as a Potential New Player in Inflammation during Rotator Cuff Tendon Injury/Repair: An In Vitro Model.International journal of molecular sciences · 2022Article
- Inhibition of Integrin αvβ6 Activation of TGF-β Attenuates Tendinopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Tendinopathy is a common tendon disorder that causes pain and impairs function. It is the most common reason for consultation with musculoskeletal specialists. The available therapies for tendinopathy are limited in number and efficacy and have unclear cellular and molecular mechanisms. Here it is shown that transforming growth factor-beta (TGF-β) activated by integrin αvβ6 promotes tendinopathy in mice. Excessive active TGF-β is found during tendinopathy progression, which led to tenocytes' phenotype transition to chondrocytes. Transgenic expression of active TGF-β in tendons induced spontaneous tendinopathy, whereas systemic injection of a TGF-β neutralizing antibody attenuated tendinopathy. Inducible knockout of the TGF-β type 2 receptor gene (Tgfbr2) in tenocytes inhibited tendinopathy progression in mice. Moreover, it is found that integrin αvβ6 induces TGF-β activation in response to mechanical load in tendons. Conditional knockout of the integrin αv gene in tendons prevented tendinopathy in mice. The study suggests that integrin αvβ6 activation of TGF-β is the mechanism of tendinopathy, and that integrin αvβ6 may be a therapeutic target in tendinopathy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.