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Background  Macrophages and Wnt proteins (Wnts) are independently involved in cardiac development, response to cardiac injury, and repair. However, the role of macrophage‐derived Wnts in the healing and repair of myocardial infarction ( MI ) is unknown. We sought to determine the role of macrophage Wnts in infarct repair.    Methods and Results  We show that the Wnt pathway is activated after  MI  in mice. Furthermore, we demonstrate that isolated infarct macrophages express distinct Wnt pathway components and are a source of noncanonical Wnts after  MI . To determine the effect of macrophage Wnts on cardiac repair, we evaluated mice lacking the essential Wnt transporter  Wntless  ( Wls ) in myeloid cells. Significantly,  Wntless‐ deficient macrophages presented a unique subset of M2‐like macrophages with anti‐inflammatory, reparative, and angiogenic properties. Serial echocardiography studies revealed that mice lacking macrophage Wnt secretion showed improved function and less remodeling 30 days after  MI . Finally, mice lacking macrophage‐ Wntless  had increased vascularization near the infarct site compared with controls.    Conclusions  Macrophage‐derived Wnts are implicated in adverse cardiac remodeling and dysfunction after  MI . Together, macrophage Wnts could be a new therapeutic target to improve infarct healing and repair.

Loss of Macrophage Wnt Secretion Improves Remodeling and Function After Myocardial Infarction in Mice