The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Tenascin-C drives persistence of organ fibrosis
Open accessAbstract
The factors responsible for maintaining persistent organ fibrosis in systemic sclerosis (SSc) are not known but emerging evidence implicates toll-like receptors (TLRs) in the pathogenesis of SSc. Here we show the expression, mechanism of action and pathogenic role of endogenous TLR activators in skin from patients with SSc, skin fibroblasts, and in mouse models of organ fibrosis. Levels of tenascin-C are elevated in SSc skin biopsy samples, and serum and SSc fibroblasts, and in fibrotic skin tissues from mice. Exogenous tenascin-C stimulates collagen gene expression and myofibroblast transformation via TLR4 signalling. Mice lacking tenascin-C show attenuation of skin and lung fibrosis, and accelerated fibrosis resolution. These results identify tenascin-C as an endogenous danger signal that is upregulated in SSc and drives TLR4-dependent fibroblast activation, and by its persistence impedes fibrosis resolution. Disrupting this fibrosis amplification loop might be a viable strategy for the treatment of SSc.
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Rockey, D. C., Bell, P. D., & Hill, J. A. (2015) · New England Journal of Medicine · doi:10.1056/nejmra1300575 · Cited by 1,428
Standardized Quantification of Pulmonary Fibrosis in Histological Samples
Hübner, R.-H., Gitter, W., Eddine El Mokhtari, N., Mathiak, M., Both, M., Bolte, H., Freitag-Wolf, S., & Bewig, B. (2008) · BioTechniques · doi:10.2144/000112729 · Cited by 817
Understanding fibrosis in systemic sclerosis: shifting paradigms, emerging opportunities
Bhattacharyya, S., Wei, J., & Varga, J. (2012) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2011.149 · Cited by 381
Self-citationWu, M., Melichian, D. S., de la Garza, M., Gruner, K., Bhattacharyya, S., Barr, L., Nair, A., Shahrara, S., Sporn, P. H. S., Mustoe, T. A., et al. (2009) · The American Journal of Pathology · doi:10.2353/ajpath.2009.090241 · Cited by 125
Self-citationStifano, G., Affandi, A. J., Mathes, A. L., Rice, L. M., Nakerakanti, S., Nazari, B., Lee, J., Christmann, R. B., & Lafyatis, R. (2014) · Arthritis Research & Therapy · doi:10.1186/ar4598 · Cited by 86
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Metadata
- Authors
- Bhattacharyya, S., Wang, W., Morales-Nebreda, L., Feng, G., Wu, M., Zhou, X., Lafyatis, R., Lee, J., Hinchcliff, M., Feghali-Bostwick, C., Lakota, K., Budinger, G. R. S., Raparia, K., Tamaki, Z., & Varga, J.
- Venue
- Nature Communications
- Published
- 2016-06-03
- Volume
- 7
- Issue
- 1
- Pages
- 11703-11703
- ISSN
- 2041-1723 (ISSN-L)
- OpenAlex
- W2411779324
- Cited by
- 292
- References
- 5
- FWCI
- 19.02
- Type
- journal article
- Language
- en
- Open access
- gold
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- Bhattacharyya, S., Wang, W., Morales-Nebreda, L., Feng, G., Wu, M., Zhou, X., Lafyatis, R., Lee, J., Hinchcliff, M., Feghali-Bostwick, C., Lakota, K., Budinger, G. R. S., Raparia, K., Tamaki, Z., & Varga, J. (2016). Tenascin-C drives persistence of organ fibrosis. Nature Communications. https://doi.org/10.1038/ncomms11703
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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