Tgfbr1, short for transforming growth factor-beta receptor 1, is a key component in the TGF-β signaling pathway. This pathway is involved in numerous biological processes such as cell growth, differentiation, and extracellular matrix production. Perturbations in TGF-β signaling can lead to various human phenotypes, highlighting the biological importance of Tgfbr1 [1].

In post-myocardial infarction mice, calycosin was found to reduce myocardial fibrosis and improve cardiac function by suppressing the Tgfbr1 signaling pathway. Deletion of Tgfbr1 in cardiac-specific knockout mice partially counteracted the beneficial effects of calycosin, suggesting that Tgfbr1 is crucial in myocardial fibrosis and cardiac dysfunction after myocardial infarction [2]. In bioengineered vascular grafts, a pathogenic TGFBR1 variant (TGFBR1A230T) led to impaired mechanical properties, aneurysm-like formation in vivo, and defects in collagen-related processes, demonstrating the role of Tgfbr1 in vascular integrity and aneurysm development [3].

In conclusion, Tgfbr1 is essential in the TGF-β signaling pathway, influencing multiple biological processes. Studies using gene-knockout mouse models have revealed its significance in diseases like myocardial fibrosis and aneurysm formation. Understanding Tgfbr1's function provides insights into the mechanisms of these diseases and may offer potential therapeutic targets.