Purpose of review: Macrophages alter their responses during the temporal stages of wound healing. During the inflammatory phase macrophages perform phagocytosis. During neovascularization macrophages activate angiogenesis. In the proliferation phase of wound healing, macrophages deposit extracellular matrix and during wound resolution macrophages phagocytize excessive cellular components. This review addresses how these changing phenotypes affect skin repair and disease.
Recent findings: Macrophages can determine the outcome of repair and can shift the normal wound healing response into fibrosis or chronic wounds. Emerging single cell technologies for the first time provide us with tools to uncover macrophage origin, heterogeneity and function.
Summary: Macrophages may exist as one population where all cells alter their phenotype in response to signals from the microenvironment. Alternatively, macrophages may exist as distinct subsets that can control wound outcomes. A clarified understanding will strengthen our knowledge of skin biology and aid in the development of wound healing therapies.
Keywords: Chronic Wounds; Heterogeneity; Macrophage Subsets; Macrophages; Skin Fibrosis; Wound Healing.