The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases
Open accessAbstract
Fibroproliferative diseases, including the pulmonary fibroses, systemic sclerosis, liver cirrhosis, cardiovascular disease, progressive kidney disease, and macular degeneration, are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Fibrotic tissue remodeling can also influence cancer metastasis and accelerate chronic graft rejection in transplant recipients. Nevertheless, despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis. The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibroproliferative diseases and to identify the common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies.
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Cites
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Bataller, R., & Brenner, D. A. (2005) · Journal of Clinical Investigation · doi:10.1172/jci24282 · Cited by 4,958
Myofibroblasts and mechano-regulation of connective tissue remodelling
Tomasek, J. J., Gabbiani, G., Hinz, B., Chaponnier, C., & Brown, R. A. (2002) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm809 · Cited by 4,290
The Versatile Role of microRNA-30a in Human Cancer
Wang, C., Yang, X., Chen, Y., & Chen, L. (2017) · Cellular Physiology and Biochemistry · doi:10.1159/000471111 · Cited by 3,409
Mesenchymal stem cells as trophic mediators
Caplan, A. I., & Dennis, J. E. (2006) · Journal of Cellular Biochemistry · doi:10.1002/jcb.20886 · Cited by 2,992
Epithelial-mesenchymal transition and its implications for fibrosis
Kalluri, R., & Neilson, E. G. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200320530 · Cited by 2,649
TRANSFORMING GROWTH FACTOR-β REGULATION OF IMMUNE RESPONSES
Li, M. O., Wan, Y. Y., Sanjabi, S., Robertson, A.-K. L., & Flavell, R. A. (2006) · Annual Review of Immunology · doi:10.1146/annurev.immunol.24.021605.090737 · Cited by 2,206
Klinge, U., Park, J.-K., & Klosterhalfen, B. (2013) · Pathobiology · doi:10.1159/000348446 · Cited by 1,783
Fibrotic disease and the TH1/TH2 paradigm
Wynn, T. A. (2004) · Nature Reviews Immunology · doi:10.1038/nri1412 · Cited by 1,765
Self-citationSelective depletion of macrophages reveals distinct, opposing roles during liver injury and repair
Duffield, J. S., Forbes, S. J., Constandinou, C. M., Clay, S., Partolina, M., Vuthoori, S., Wu, S., Lang, R., & Iredale, J. P. (2005) · Journal of Clinical Investigation · doi:10.1172/jci200522675 · Cited by 1,649
Cited by
Cellular and molecular mechanisms of fibrosis
Wynn, T. (2008) · The Journal of Pathology · doi:10.1002/path.2277 · Cited by 4,495
Self-citationMacrophages in Tissue Repair, Regeneration, and Fibrosis
Wynn, T. A., & Vannella, K. M. (2016) · Immunity · doi:10.1016/j.immuni.2016.02.015 · Cited by 4,481
Self-citationCox, T. R., & Erler, J. T. (2011) · Disease Models & Mechanisms · doi:10.1242/dmm.004077 · Cited by 1,569
Fibrosis–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
Macrophages: master regulators of inflammation and fibrosis
Wynn, T., & Barron, L. (2010) · Seminars in Liver Disease · doi:10.1055/s-0030-1255354 · Cited by 1,392
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Metadata
- Authors
- Wynn, T. A.
- Venue
- Journal of Clinical Investigation
- Published
- 2007-03-01
- Volume
- 117
- Issue
- 3
- Pages
- 524-529
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W1981269419
- Cited by
- 1,456
- References
- 52
- FWCI
- 47.91
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
