Gata6, also known as GATA-binding factor 6, is a zinc-finger transcriptional regulator. It belongs to the GATA family, which plays key roles in cell fate determination, proliferation, migration, and organogenesis of endoderm-and mesoderm-derived organs in vertebrates. Gata6 is involved in various biological processes such as immune regulation, organ development, and is associated with multiple disease-related pathways [4,5]. Genetic models, especially KO/CKO mouse models, are valuable for studying its functions.

In arterial calcification, knockdown of Gata6 via recombinant adeno-associated virus carrying GATA6 shRNA inhibited the development of arterial calcification in mice with chronic kidney disease (CKD). Gata6 was found to accelerate vascular smooth muscle cell (VSMC) senescence-related arterial calcification by counteracting the anti-aging factor SIRT6 and impeding DNA damage repair [1]. In pancreatic cancer, Gata6 expression can distinguish classical and basal-like subtypes, with basal-like tumors being chemoresistant. Gata6 expression is prognostic in a multivariate analysis [2]. In the heart, disruption of the pericardial cavity, where Gata6 + macrophages are located, accelerated maladaptive post-myocardial infarction (MI) cardiac remodeling. These macrophages relocate to the injured heart and prevent cardiac fibrosis [3].

In conclusion, Gata6 is essential in multiple biological processes. Model-based research, especially KO/CKO mouse models, has revealed its significant roles in diseases like arterial calcification, pancreatic cancer, and post-MI cardiac remodeling. Understanding Gata6's functions provides potential new targets for intervention in these disease areas.