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 Fpn inactivation in macrophages led to transient alopecia and impaired hair follicle growth due to local iron distribution issues, which caused cellular iron deprivation and reduced proliferation in adjacent epithelial cells. This hair loss was not linked to hypoferremia or anemia. Additionally, Fpn deletion resulted in delayed skin wound healing, with defective granulation tissue formation and impaired blood vessel development, although it did not affect inflammation or immune cell recruitment. In the context of liver fibrosis, Fpn inactivation did not impact inflammation or fibrogenesis but showed a different susceptibility to liver damage, as indicated by lower transaminase levels. The study concluded that macrophage trophic functions in skin homeostasis and healing are dependent on iron and Fpn, highlighting the need for further exploration of these mechanisms in different fibrosis models.