Tgfbr2, the type II receptor of the transforming growth factor beta (TGF-β) signaling pathway, is crucial for regulating various biological processes. The TGF-β signaling pathway, in which Tgfbr2 is a key component, is involved in processes like cell growth, differentiation, apoptosis, and extracellular matrix remodeling. Genetic models, such as knockout (KO) or conditional knockout (CKO) mouse models, have been instrumental in studying its functions [1,2,3].

In Marfan syndrome (MFS) research, Piezo1 conditional knockout in MFS mice (MFS × CKO) showed that PIEZO1 deficiency aggravates MFS aneurysms by promoting TGF-β signaling pathway activation via inhibiting Tgfbr2 endocytosis and autophagy, suggesting Tgfbr2's role in MFS-related aneurysm development [1]. In lung squamous cell carcinoma (SCC) studies, loss of Tgfbr2 in KrasG12D mice led to predominant lung SCC development with short latency, high penetrance, and extensive metastases, revealing its significance in suppressing SCC formation [3].

In conclusion, Tgfbr2 is essential for the normal operation of the TGF-β signaling pathway and thus for numerous biological processes. Research using KO/CKO mouse models has demonstrated its significance in diseases like Marfan syndrome-related aneurysms and lung squamous cell carcinoma, enhancing our understanding of disease mechanisms and potentially paving the way for new treatment strategies.