AI Article Synopsis
- TGF-β is important for early development, immune responses, tissue repair, and maintaining balance in adult organisms, but its role in fibrosis and cancer is complicated—sometimes helping and other times hindering the disease process.
- Overproduction of TGF-β can lead to harmful changes in tissues, like epithelial-mesenchymal transition and increased extracellular matrix, contributing to fibrosis and cancer progression.
- Targeting TGF-β for treatment shows promise, but potential side effects and toxicity have made it challenging to develop effective therapies.
Article Abstract
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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9033932 | PMC |
| http://dx.doi.org/10.1186/s12943-022-01569-x | DOI Listing |
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