DPYSL2 and myocardial infarction: In ApoE−/− mice with MI, nanoparticle-mediated delivery of CRMP2 siRNA to wound macrophages efficiently suppressed expression of CRMP2 in vivo, associated with reduced expression of inflammatory M1 macrophage markers, increased resolution of inflammation, accelerated infarct healing, and attenuated fibrosis, development of post-MI heart failure and mortality.