Indeed, macrophages with deletion of Ndufs4, encoding a member of mitochondrial respiratory complex I, assume a proinflammatory phenotype with increased glycolytic activity and reduced mitochondrial function, while Ndufs4 knock-out mice presented with suppressed efferocytosis and a delayed transition of proinflammatory to reparatory macrophages after MI, which was associated with increased scarring, thinner LV walls, and compromised repair after MI [108]. This evidence concerns the gene NDUFS4 and myocardial infarction.