Accordingly, we used the angiotensin II (Ang II)-infused mouse model of non-ischemic cardiac fibrosis, as well as in vitro cell models, to determine the contribution of Nr4a1 to: (1) cardiac fibrosis and diastolic dysfunction; (2) macrophage phenotype and function; (3) macrophage-fibroblast interactions; and (4) cardiac fibroblast phenotype and function. Here, AGT is linked to fibrosis.