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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Regulation of Wound Healing by Growth Factors and Cytokines
WERNER, S., & GROSE, R. (2003) · Physiological Reviews · doi:10.1152/physrev.2003.83.3.835 · Cited by 3,629
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Massagué, J., & Chen, Y. (2000) · PubMed · Cited by 1,780
Controlling TGF-β signalingPreprint
Massagué, J., & Chen, Y. (2000) · Genes & Development · doi:10.1101/gad.14.6.627 · Cited by 1,589
Brooks, P. C., Strömblad, S., Sanders, L. C., Schalscha, T. V., Aimes, R. T., Stetler‐Stevenson, W. G., Quigley, J. P., & Cheresh, D. A. (1996) · Cell · doi:10.1016/s0092-8674(00)81235-0 · Cited by 1,566
Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix
Wipff, P.-J., Rifkin, D. B., Meister, J.-J., & Hinz, B. (2007) · The Journal of Cell Biology · doi:10.1083/jcb.200704042 · Cited by 1,346
TGFβ: the molecular Jekyll and Hyde of cancer
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Cellular and molecular mechanisms of renal fibrosis
Liu, Y. (2011) · Nature Reviews Nephrology · doi:10.1038/nrneph.2011.149 · Cited by 1,483
“Integrins are a family of heterodimeric transmembrane receptors that consist of α and β subunits and bind to the ECM and to the cytoskeleton, thereby integrating the 'outside-in' and 'inside-out' signals between cells and their extracellular environment”
BackgroundFibrosis–a common pathway to organ injury and failure
Rockey, D. C., Bell, P. D., & Hill, J. A. (2015) · New England Journal of Medicine · doi:10.1056/nejmra1300575 · Cited by 1,428
Extracellular matrix: A dynamic microenvironment for stem cell niche
Gattazzo, F., Urciuolo, A., & Bonaldo, P. (2014) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2014.01.010 · Cited by 1,365
Combination cancer immunotherapy and new immunomodulatory targets
Mahoney, K. M., Rennert, P. D., & Freeman, G. J. (2015) · Nature Reviews Drug Discovery · doi:10.1038/nrd4591 · Cited by 1,294
Transforming growth factor–β in tissue fibrosis
Frangogiannis, N. G. (2019) · The Journal of Experimental Medicine · doi:10.1084/jem.20190103 · Cited by 1,354
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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