We demonstrate that Opn is expressed in a subset of macrophages at the injury, with an increase in spp1+ cardiac macrophages at 7 dpi, a reciprocal expression pattern from that observed for tnfα. Studies in mammals have described contradictory roles for OPN in controlling macrophage phenotype; it may be a marker of alternatively activated ‘M2’ macrophages in the mouse heart24 but loss of OPN promotes a more anti-inflammatory phenotype in a model of muscular dystrophy.51 Here, SPP1 is linked to muscular dystrophy.