An injured heart remains scarred and deformed (right) when it is unable to recruit a clean-up crew of inflammatory monocytes.
Circulating monocytes recruited to an injured heart break down dead cells and scoop up their toxic products. This inflammation is followed by reconstruction, when monocyte cytokines promote blood vessel growth and recruit healing fibroblasts.
Previous studies suggested that a single monocyte population accomplishes both these functions by switching from clean-up mode to repair mode. But the recent identification of two monocyte subsets in the circulation, only one of which is inflammatory, implies otherwise. Each subset has its own unique receptors that respond to different chemokine signals.
Nahrendorf et al. now find that damaged hearts in mice recruit the two subsets in turn by secreting only one chemokine at a time. The first chemokine drew in inflammatory monocytes, which accumulated in the injured heart for three days and then disappeared. The pro-repair subset arrived later to help rebuild the heart.
Mice suffering from atherosclerosis—the main cause of human heart failure—have many inflammatory monocytes. Their injured hearts thus remained scarred and deformed. It is possible that a similar imbalance in humans predisposes these individuals to heart failure. 
