TRIB1 and myocardial infarction: In particular, macrophage depletion is deleterious to infarct healing and worsens the remodeling process.34,35 Despite being merely 2–5% of the total macrophage population in the heart in the initial weeks post-MI, the depletion of cardiac resident macrophages impaired normal infarct healing and adversely affected the remodeling process.5 Shiraishi et al. demonstrated the effect of inactivation of alternatively activated (M2) macrophages post-MI by using a mouse model with Trib1 gene deletion.36 The impaired wound remodeling was rescued by the introduction of M2 macrophages exogenously.