Targeting TGF-β signal transduction for fibrosis and cancer therapy

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. However, due to potential systemic cytotoxicity, the development of TGF-β therapeutics has lagged.

⚡ This is an original paraphrased summary — not copied from the abstract. Full paper available at the source link below.

• 1 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.
• 2 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.
• 3 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.

Understanding this could lead to better treatments, improved diagnostics, or a deeper grasp of how the human body works — benefiting patient care globally.

This summary is based on publicly available metadata and abstract. For the full research paper, visit the original source: