Myeloid cell-specific EGFR deletion leads to increased cardiomyocyte hypertrophy and worsened cardiac function and repair after acute myocardial infarction, with decreased levels of pro-reparative mediators such as Vegfa and Il10, and reduced capillary density.592 In addition to EGFR, inflammatory cells secrete myeloid-derived growth factor (MYDGF) to aid tissue repair and regeneration following acute myocardial infarction. Here, MYDGF is linked to myocardial infarction.