It has been suggested that dying cardiomyocytes release DAMPs which interact with pattern recognition receptors, in particular Toll-like receptors (TLRs) expressed by neighboring cardiomyocytes, fibroblasts, immune cells and parenchymal cells to initiate fibrosis (43); fibroblasts, macrophages and CD4+ T cells all contribute to cardiac fibrosis that develops in non-ischemic hypertensive hearts (16, 17, 56). Here, CD4 is linked to fibrosis.