Particularly, the 1,000 group also upregulated Axl expression, which is involved in Mφ efferocytosis and can further increase intramyocardial inflammation (Figures 4C–I) (DeBerge et al., 2021) Besides, our histological assays showed that the 250 and 1,000 groups differentially exhibited reduction of chronic inflammation at the infarct, ameliorated LV fibrosis, and, to a minor extent, enhanced revascularization, all of which potentially contributed to the improved LV contractile function and remodeling (Figures 5–7). This evidence concerns the gene AXL and fibrosis.