Thus, we sought to compare HFpEF fibroblast activation with other cardiac fibrotic disease etiologies by integration of our single-cell data with two other single-cell resources that represent different types of HFrEF: first, a model for cardiac fibrosis and hypertrophy by hypertensive stress induced by 2 weeks of angiotensin II (AngII) administration [62] and second, an acute myocardial infarction (MI) model [31] that assessed early (< day 7) and later ischemic remodeling (day 7–14) (Fig. 2A). This evidence concerns the gene AGT and myocardial infarction.