CCR2 and persistent truncus arteriosus: As an example, antibody-based depletion of CCR2+ monocyte-derived macrophages, a recruited population in early PO, 3 to 5 days following TAC, was shown to protect the myocardium from pathological remodeling and progression to interstitial fibrosis demonstrating that recruited macrophages, CCR2+ and Ly6Chigh, exacerbate the remodeling response to PO [47].