The DOI matches its Crossref record; 81 of the 81 references it cites were found in a registry or an index.
Integrin–TGF‐β crosstalk in fibrosis, cancer and wound healing
Open accessAbstract
Accumulating evidence indicates that there is extensive crosstalk between integrins and TGF-beta signalling. TGF-beta affects integrin-mediated cell adhesion and migration by regulating the expression of integrins, their ligands and integrin-associated proteins. Conversely, several integrins directly control TGF-beta activation. In addition, a number of integrins can interfere with both Smad-dependent and Smad-independent TGF-beta signalling in different ways, including the regulation of the expression of TGF-beta signalling pathway components, the physical association of integrins with TGF-beta receptors and the modulation of downstream effectors. Reciprocal TGF-beta-integrin signalling is implicated in normal physiology, as well as in a variety of pathological processes including systemic sclerosis, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease and cancer; thus, integrins could provide attractive therapeutic targets to interfere with TGF-beta signalling in these processes.
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“By disrupting mechanical force transmission between cells and the ECM, integrin inhibitors not only attenuate TGF-b activation but also modulate immune cell adhesion and migration, effectively dampening pro-fibrotic inflammation at its source (129).”
From The mechanotransduction-immune axis in organ fibrosis: dual regulatory mechanisms and translational therapeutic perspectives (2025) · cites this paper as [129]
In the citing paper
“integrins are known to activate TGF-β”
From Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway (2017) · cites this paper as Margadant and Sonnenberg, 2010
In the citing paper
“Accumulating evidence indicates that a cross-talk between integrins and TGF-β exists, in particular to regulate fibrosis, wound healing, and cancer (Asano et al., 2005, Margadant and Sonnenberg, 2010).”
From Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway (2017) · cites this paper as Margadant and Sonnenberg, 2010
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Metadata
- Authors
- Margadant, C., & Sonnenberg, A.
- Affiliations
- The Netherlands Cancer Institute (NL)
- Corresponding author
- Sonnenberg, Arnoud
- Venue
- The EMBO Reports
- Published
- 2010-01-15
- Volume
- 11
- Issue
- 2
- Pages
- 97-105
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC2828749
- OpenAlex
- W2112195516
- Cited by
- 653
- References
- 81
- Citations by year
- 2026: 28 · 2025: 50 · 2024: 32 · 2023: 41 · 2022: 30 · 2021: 38 · 2020: 41 · 2019: 34 · 2018: 45 · 2017: 38 · 2016: 45 · 2015: 43 · 2014: 49 · 2013: 36 · 2012: 51
- FWCI
- 3.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- EMBO Reports (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- European Molecular Biology Organization
- Dystrophic Epidermolysis Bullosa Research Association
- KWF Kankerbestrijding
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Keywords
- TGF-beta signaling, integrins, Smad signaling, TGF-beta receptor, cell adhesion, cell migration, fibrosis, systemic sclerosis, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, cancer, wound healing, therapeutic target
- MeSH terms
- Animals, Fibrosis, Humans, Models, Biological, Neoplasms, Wound Healing, Integrins, Transforming Growth Factor beta, Disease Progression, Receptor Cross-Talk
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