Myeloid ALX/FPR2 Regulates Vascularization Following Tissue Injury

Mechanistically, RNA sequencing revealed that resolvin D1 induced a transcriptional program in macrophages characteristic of a pro-revascularization phenotype. Vascularization of ischemic skeletal muscle, as well as cutaneous wounds, was impaired in mice with myeloid-specific deficiency of Alx/Fpr2, and this was associated with altered expression of pro-revascularization genes in skeletal muscle and macrophages isolated from skeletal muscle.