The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
New insights into TGF-β/Smad signaling in tissue fibrosis
Open accessAbstract
Transforming growth factor-β1 (TGF-β1) is considered as a crucial mediator in tissue fibrosis and causes tissue scarring largely by activating its downstream small mother against decapentaplegic (Smad) signaling. Different TGF-β signalings play different roles in fibrogenesis. TGF-β1 directly activates Smad signaling which triggers pro-fibrotic gene overexpression. Excessive studies have demonstrated that dysregulation of TGF-β1/Smad pathway was an important pathogenic mechanism in tissue fibrosis. Smad2 and Smad3 are the two major downstream regulator that promote TGF-β1-mediated tissue fibrosis, while Smad7 serves as a negative feedback regulator of TGF-β1/Smad pathway thereby protects against TGF-β1-mediated fibrosis. This review presents an overview of the molecular mechanisms of TGF-β/Smad signaling pathway in renal, hepatic, pulmonary and cardiac fibrosis, followed by an in-depth discussion of their molecular mechanisms of intervention effects both in vitro and in vivo. The role of TGF-β/Smad signaling pathway in tumor or cancer is also discussed. Additionally, the current advances also highlight targeting TGF-β/Smad signaling pathway for the prevention of tissue fibrosis. The review reveals comprehensive pathophysiological mechanisms of tissue fibrosis. Particular challenges are presented and placed within the context of future applications against tissue fibrosis.
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Heidenreich, P. A., Trogdon, J. G., Khavjou, O. A., Butler, J., Dracup, K., Ezekowitz, M. D., Finkelstein, E. A., Hong, Y., Johnston, S. C., Khera, A., et al. (2011) · Circulation · doi:10.1161/cir.0b013e31820a55f5 · Cited by 3,208
Lederer, D. J., & Martinez, F. J. (2018) · New England Journal of Medicine · doi:10.1056/nejmra1705751 · Cited by 2,056
Signaling Receptors for TGF-β Family Members
Heldin, C.-H., & Moustakas, A. (2016) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a022053 · Cited by 711
Integrin–TGF‐β crosstalk in fibrosis, cancer and wound healing
Margadant, C., & Sonnenberg, A. (2010) · The EMBO Reports · doi:10.1038/embor.2009.276 · Cited by 653
The role of TGF-β/SMAD4 signaling in cancer
Zhao, M., Mishra, L., & Deng, C.-X. (2018) · International Journal of Biological Sciences · doi:10.7150/ijbs.23230 · Cited by 631
Regulation of the Bioavailability of TGF-β and TGF-β-Related Proteins
Robertson, I. B., & Rifkin, D. B. (2016) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a021907 · Cited by 403
Transcriptional Control by the SMADs
Hill, C. S. (2016) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a022079 · Cited by 351
TGF-β family co-receptor function and signaling
Nickel, J., Ten Dijke, P., & Mueller, T. D. (2018) · Acta Biochimica et Biophysica Sinica · doi:10.1093/abbs/gmx126 · Cited by 198
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Therapeutic Potential of Centella asiatica and Its Triterpenes: A Review
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Pei, Z., Qin, Y., Fu, X., Yang, F., Huo, F., Liang, X., Wang, S., Cui, H., Lin, P., Zhou, G., et al. (2022) · Redox Biology · doi:10.1016/j.redox.2022.102509 · Cited by 269
TGF-β as A Master Regulator of Aging-Associated Tissue Fibrosis
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Metadata
- Authors
- Hu, H.-H., Chen, D.-Q., Wang, Y.-N., Feng, Y.-L., Cao, G., Vaziri, N. D., & Zhao, Y.-Y.
- Venue
- Chemico-Biological Interactions
- Publisher
- Elsevier BV
- Published
- 2018-08
- Volume
- 292
- Pages
- 76-83
- ISSN
- 0009-2797 (ISSN-L)
- OpenAlex
- W2881438881
- Cited by
- 1,179
- References
- 8
- FWCI
- 23.46
- Type
- journal article
- Language
- en
- Open access
- green
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- Hu, H.-H., Chen, D.-Q., Wang, Y.-N., Feng, Y.-L., Cao, G., Vaziri, N. D., & Zhao, Y.-Y. (2018). New insights into TGF-β/Smad signaling in tissue fibrosis. Chemico-Biological Interactions. https://doi.org/10.1016/j.cbi.2018.07.008
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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).
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