The DOI matches its Crossref record; 218 of the 218 references it cites were found in a registry or an index.
Targeting TGF-β signal transduction for fibrosis and cancer therapy
Open accessAbstract
Transforming growth factor β (TGF-β) has long been identified with its intensive involvement in early embryonic development and organogenesis, immune supervision, tissue repair, and adult homeostasis. The role of TGF-β in fibrosis and cancer is complex and sometimes even contradictory, exhibiting either inhibitory or promoting effects depending on the stage of the disease. Under pathological conditions, overexpressed TGF-β causes epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) deposition, cancer-associated fibroblast (CAF) formation, which leads to fibrotic disease, and cancer. Given the critical role of TGF-β and its downstream molecules in the progression of fibrosis and cancers, therapeutics targeting TGF-β signaling appears to be a promising strategy. However, due to potential systemic cytotoxicity, the development of TGF-β therapeutics has lagged. In this review, we summarized the biological process of TGF-β, with its dual role in fibrosis and tumorigenesis, and the clinical application of TGF-β-targeting therapies.
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2 retracted
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Antar, S. A., Ashour, N. A., Marawan, M. E., & Al-Karmalawy, A. A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24044004 · Cited by 366
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Xiao, Z., Todd, L., Huang, L., Noguera-Ortega, E., Lu, Z., Huang, L., Kopp, M., Li, Y., Pattada, N., Zhong, W., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-40850-5 · Cited by 272
Metadata
- Authors
- Peng, D., Fu, M., Wang, M., Wei, Y., & Wei, X.
- Venue
- Molecular Cancer
- Published
- 2022-04-23
- Volume
- 21
- Issue
- 1
- Pages
- 104-104
- ISSN
- 1476-4598 (ISSN-L)
- OpenAlex
- W4224221174
- Cited by
- 1,065
- References
- 218
- FWCI
- 57.73
- Type
- journal article
- Language
- en
- Open access
- gold
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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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