Our results demonstrate for the first time that cardiomyocyte-specific transgenic overexpression of GRK5 not only enhanced the acute immune cell recruitment response post-MI to the heart (macrophages, mast cells, and pro-inflammatory neutrophils) but also led to chronic immune cell infiltration after the establishment of HF (neutrophils, macrophages, and T-cells). Here, GRK5 is linked to myocardial infarction.