Tgfbi, also known as transforming growth factor beta-induced gene, codes for an extracellular matrix protein TGFBIp. It is involved in multiple biological processes. In the corneal stroma, it's the second-most abundant protein. It may participate in pathways related to cell-matrix interactions, and its dysregulation is associated with various diseases, highlighting its biological importance. Genetic models, such as KO/CKO mouse models, are valuable for studying its functions [2].

In pancreatic cancer, TGFBI produced by tumor-associated macrophages (TAMs) promotes M2 polarization of macrophages and pancreatic cancer growth. Loss-of-function of TGFBI in macrophages inhibited M2 polarization, MΦ-mediated pancreatic cancer growth, and enhanced anti-tumor immunity, sensitizing pancreatic cancer to chemotherapy [1]. In breast cancer, deletion of Tgfbi in a mouse model led to a decrease in cancer stem cell (CSC) content and lung metastasis, with improved vessel perfusion and decreased hypoxia in tumors [3]. In pulmonary arterial hypertension, TGFBI is upregulated in monocrotaline-induced PAH, and its expression is associated with endothelial-to-mesenchymal transition (EndMT). Treatment with bosentan reversed the pathological changes related to TGFBI and EndMT [4].

In conclusion, Tgfbi plays crucial roles in multiple disease-related biological processes. Studies using KO/CKO mouse models have revealed its functions in pancreatic cancer, breast cancer, and pulmonary arterial hypertension, providing insights into potential therapeutic strategies for these diseases.