Iron is an essential
trace element in the metabolism of almost all living organisms.
Iron overload can disrupt bone homeostasis by significant inhibition of osteogenic differentiation and stimulation of osteoclastogenesis, consequently leading to
osteoporosis.
Iron accumulation is also involved in the
osteoporosis induced by multiple factors, such as
estrogen deficiency, ionizing radiation, and mechanical unloading.
Iron chelators are first developed for treating
iron overloaded disorders. However, growing evidence suggests that
iron chelators can be potentially used for the treatment of bone loss. In this review, we focus on the
therapeutic effects of
iron chelators on bone loss.
Iron chelators have
therapeutic effects not only on
iron overload induced
osteoporosis, but also on
osteoporosis induced by
estrogen deficiency, ionizing radiation, and mechanical unloading, and in
Alzheimer's disease-associated osteoporotic deficits.
Iron chelators differently affect the cellular behaviors of bone cells. For osteoblast lineage cells (bone mesenchymal stem cells and osteoblasts),
iron chelation stimulates osteogenic differentiation. Conversely,
iron chelation significantly inhibits osteoclast differentiation. These different responses may be associated with the different needs of
iron during differentiation.
Fibroblast growth factor 23, angiogenesis, and
antioxidant capability are also involved in the osteoprotective effects of
iron chelators.