Rauner Martina
Department of Medicine III & Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany.
Adv Exp Med Biol. 2025;1480:311-325. doi: 10.1007/978-3-031-92033-2_20.
Clinical and preclinical studies indicate that unbalanced systemic iron concentrations negatively affect bone health. Despite distinct underlying mechanisms, both iron deficiency and iron overload result in decreased bone mineral density and an increased fracture risk, the latter being associated with higher morbidity and mortality rates. In iron deficiency, both osteoclasts and osteoblasts suffer from the lack of iron to efficiently execute metabolic processes and produce enough energy for bone resorption and formation, respectively. In contrast, iron overload inhibits osteoblast differentiation and function by increasing the production of reactive oxygen species and lipid peroxidation, while it stimulates osteoclastogenesis and bone resorption. Besides the direct effects of iron on bone, regulators of systemic iron homeostasis have also been shown to impact bone homeostasis. This chapter summarizes current knowledge on the regulation of bone cell function and bone homeostasis by iron. Furthermore, it discusses new avenues for the treatment of iron-related bone loss.
临床和临床前研究表明,全身铁浓度失衡会对骨骼健康产生负面影响。尽管潜在机制不同,但缺铁和铁过载都会导致骨密度降低和骨折风险增加,后者与更高的发病率和死亡率相关。在缺铁状态下,破骨细胞和成骨细胞都因缺乏铁而难以有效执行代谢过程,分别无法为骨吸收和骨形成产生足够能量。相比之下,铁过载通过增加活性氧的产生和脂质过氧化来抑制成骨细胞分化和功能,同时刺激破骨细胞生成和骨吸收。除了铁对骨骼的直接影响外,全身铁稳态的调节因子也已被证明会影响骨稳态。本章总结了目前关于铁对骨细胞功能和骨稳态调节的认识。此外,还讨论了治疗铁相关骨质流失的新途径。