Hepcidin knockout exacerbates hindlimb unloading-induced bone loss in mice through inhibiting osteoblastic differentiation.

ABSTRACT:

Background

An oligopeptide hepcidin is encoded by the human HAMP gene (Hamp in mice). Its deficiency can result in iron overload, while excess may lead to iron deficiency. Hepcidin knockout mice exhibited iron accumulation in multiple tissues, accompanied by degeneration of bone microarchitecture and reduced biomechanical properties. Astronauts who are exposed to weightlessness during prolonged spaceflight experience bone loss. After space missions, an interrelation exists between iron stores and bone mineral density (BMD). Bone loss in mice due to unloading is linked to iron excess and involves hepcidin. The potential role of hepcidin in unloading-induced bone loss remains unclear.

Methods

Our study conducted relevant experiments using hepcidin knockout mice and their prima

SUBMITTER: Chen X 

PROVIDER: S-EPMC11917043 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature