Mouse Hepcidin (HAMP) Protein

Background

Hepcidin Antimicrobial Peptide (HAMP) is a small, liver-derived peptide hormone that serves as the master regulator of systemic iron homeostasis and possesses antimicrobial properties. Hepcidin controls iron levels by binding to the iron export protein ferroportin, leading to its internalization and degradation, thereby reducing iron release from enterocytes, macrophages, and hepatocytes into the bloodstream. This regulation is critical for preventing iron overload and ensuring adequate iron availability for erythropoiesis. HAMP expression is modulated by factors such as systemic iron levels, inflammation, erythropoietic demand, and hypoxia. Inflammatory cytokines, particularly IL-6, stimulate HAMP production via the JAK-STAT pathway, contributing to the anemia of chronic disease by sequestering iron in storage sites. Conversely, inadequate HAMP expression leads to conditions such as hereditary hemochromatosis and iron-loading anemias. In addition to its role in iron metabolism, HAMP exhibits antimicrobial activity by directly targeting bacterial pathogens, making it a key component of the innate immune response. Therapeutic manipulation of HAMP is being explored for treating iron disorders and related conditions.