Role of Ferroportin-Mediated Iron Release from Macrophages in Tissue Homeostasis and Repair

The study explored the role of ferroportin (Fpn)-mediated iron release from macrophages in tissue homeostasis and repair, using a mouse model with impaired iron release due to Fpn deletion. It was found that mice with loss of macrophage Fpn experienced transient alopecia due to impaired hair follicle growth, linked to local iron distribution issues and decreased proliferation in adjacent epithelial cells. This hair loss was not related to anemia. Additionally, Fpn deletion led to delayed skin wound healing, with impaired blood vessel formation and stromal cell proliferation, but did not affect inflammation or liver fibrosis in a non-alcoholic steatohepatitis model. The findings suggested that macrophage trophic function in skin homeostasis and healing was dependent on iron and Fpn.