Gata4, or GATA Binding Protein 4, is a transcription factor expressed in multiple cardiovascular lineages and is essential for heart development. It also plays roles in embryonic hepatic stellate cell quiescence and is involved in pathways related to tissue fibrosis, atherosclerosis, and cell-lineage commitment [1,2,3,4]. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying Gata4's functions.

In adult mice, lack of Gata4 caused hepatic stellate cell activation and liver fibrosis, while its overexpression in hepatic stellate cells promoted liver fibrosis regression in CCl4-treated mice, suggesting Gata4 is crucial in the regulation of liver fibrosis through hepatic stellate cell deactivation [1]. In endothelial cells, Gata4-Twist1 signalling promoted EC dysfunction and atherosclerosis development as shown by in vivo and in vitro studies using Gata4-specific siRNA and EC-specific Gata4 KO mice [2]. In breast cancer, Gata4 acts as a tumor suppressor, reducing the transcription of MMP9 and hampering breast cancer metastasis in a mouse model [5].

In conclusion, Gata4 is essential for heart development and plays important roles in liver fibrosis, atherosclerosis, and breast cancer metastasis. Studies using KO or CKO mouse models have revealed its functions in these biological processes and disease conditions, providing insights into potential therapeutic targets for related diseases.