The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index.
Potential Therapeutic Targets for Cardiac Fibrosis: TGFβ, Angiotensin, Endothelin, CCN2, and PDGF, Partners in Fibroblast Activation
Abstract
Abstract : Fibrosis is one of the largest groups of diseases for which there is no therapy but is believed to occur because of a persistent tissue repair program. During connective tissue repair, “activated” fibroblasts migrate into the wound area, where they synthesize and remodel newly created extracellular matrix. The specialized type of fibroblast responsible for this action is the α-smooth muscle actin (α-SMA)–expressing myofibroblast. Abnormal persistence of the myofibroblast is a hallmark of fibrotic diseases. Proteins such as transforming growth factor (TGF)β, endothelin-1, angiotensin II (Ang II), connective tissue growth factor (CCN2/CTGF), and platelet-derived growth factor (PDGF) appear to act in a network that contributes to myofibroblast differentiation and persistence. Drugs targeting these proteins are currently under consideration as antifibrotic treatments. This review summarizes recent observations concerning the contribution of TGFβ, endothelin-1, Ang II, CCN2, and PDGF and to fibroblast activation in tissue repair and fibrosis and the potential utility of agents blocking these proteins in affecting the outcome of cardiac fibrosis.
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1 retracted
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Mechanism of Action and In Vivo Role of Platelet-Derived Growth Factor
Heldin, C.-H., & Westermark, B. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.4.1283 · Cited by 2,496
TGF-β signaling and the fibrotic response
Leask, A., & Abraham, D. J. (2004) · The FASEB Journal · doi:10.1096/fj.03-1273rev · Cited by 2,319
Self-citationHinz, B., Phan, S. H., Thannickal, V. J., Galli, A., Bochaton-Piallat, M.-L., & Gabbiani, G. (2007) · The American Journal of Pathology · doi:10.2353/ajpath.2007.070112 · Cited by 2,068
The myofibroblast in wound healing and fibrocontractive diseases
Gabbiani, G. (2003) · The Journal of Pathology · doi:10.1002/path.1427 · Cited by 1,630
Accelerated Healing of Incisional Wounds in Rats Induced by Transforming Growth Factor-β
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Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response
Ashcroft, G. S., Yang, X., Glick, A. B., Weinstein, M., Letterio, J. J., Mizel, D. E., Anzano, M., Greenwell-Wild, T., Wahl, S. M., Deng, C., et al. (1999) · Nature Cell Biology · doi:10.1038/12971 · Cited by 911
Regulation of PDGF and its receptors in fibrotic diseases
Bonner, J. C. (2004) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2004.03.006 · Cited by 768
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Cited by
Cardiac Fibrosis: The Fibroblast Awakens
Travers, J. G., Kamal, F. A., Robbins, J., Yutzey, K. E., & Blaxall, B. C. (2016) · Circulation Research · doi:10.1161/circresaha.115.306565 · Cited by 1,596
Frangogiannis, N. G. (2021) · Cardiovascular Research · doi:10.1093/cvr/cvaa324 · Cited by 1,229
Recent Developments in Myofibroblast Biology
Hinz, B., Phan, S. H., Thannickal, V. J., Prunotto, M., Desmoulière, A., Varga, J., De Wever, O., Mareel, M., & Gabbiani, G. (2012) · The American Journal of Pathology · doi:10.1016/j.ajpath.2012.02.004 · Cited by 1,193
Fibroblast-specific TGF-β–Smad2/3 signaling underlies cardiac fibrosis
Khalil, H., Kanisicak, O., Prasad, V., Correll, R. N., Fu, X., Schips, T., Vagnozzi, R. J., Liu, R., Huynh, T., Lee, S.-J., et al. (2017) · Journal of Clinical Investigation · doi:10.1172/jci94753 · Cited by 905
Skin tissue engineering: wound healing based on stem-cell-based therapeutic strategies
Nourian Dehkordi, A., Mirahmadi Babaheydari, F., Chehelgerdi, M., & Raeisi Dehkordi, S. (2019) · Stem Cell Research & Therapy · doi:10.1186/s13287-019-1212-2 · Cited by 533
Metadata
- Authors
- Leask, A.
- Venue
- Circulation Research
- Published
- 2010-06-11
- Volume
- 106
- Issue
- 11
- Pages
- 1675-1680
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2057386289
- Cited by
- 667
- References
- 66
- FWCI
- 32.91
- Type
- journal article
- Language
- en
- Open access
- closed
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- Leask, A. (2010). Potential Therapeutic Targets for Cardiac Fibrosis: TGFβ, Angiotensin, Endothelin, CCN2, and PDGF, Partners in Fibroblast Activation. Circulation Research. https://doi.org/10.1161/circresaha.110.217737
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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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