Figure 1. Hypothetical illustration of macrophage involvement in skeletal muscle aging and repair. Most resident macrophages in steady-state skeletal muscle polarize to M2 subtype. IL4, IL13 and adiponectin produced by IMAT and some still unknown factors are responsible for this skewed polarization. Polarized M2 macrophages promote collagen synthesis and adipogenesis most likely through FAPs (Fibro-adipogenic progenitors). Elevated collagen and fat are the major features of skeletal muscle aging, along with a loss of muscle mass. Increased fat may in turn promote M2 polarization by producing M2 inducing factors, which may result in M2 increase in old skeletal muscle. Upon injury, monocytes and macrophages infiltrate to the injury site and polarize to M1 to eliminate pathogens and cleanup debris. M1 switches to M2, which promotes collagen synthesis at the injury site for the repair.