Jeney Viktória
Department of Medicine, University of Debrecen Debrecen, Hungary.
Front Pharmacol. 2017 Feb 21;8:77. doi: 10.3389/fphar.2017.00077. eCollection 2017.
Diseases/conditions with diverse etiology, such as hemoglobinopathies, hereditary hemochromatosis and menopause, could lead to chronic iron accumulation. This condition is frequently associated with a bone phenotype; characterized by low bone mass, osteoporosis/osteopenia, altered microarchitecture and biomechanics, and increased incidence of fractures. Osteoporotic bone phenotype constitutes a major complication in patients with iron overload. The purpose of this review is to summarize what we have learnt about iron overload-associated bone loss from clinical studies and animal models. Bone is a metabolically active tissue that undergoes continuous remodeling with the involvement of osteoclasts that resorb mineralized bone, and osteoblasts that form new bone. Growing evidence suggests that both increased bone resorption and decreased bone formation are involved in the pathological bone-loss in iron overload conditions. We will discuss the cellular and molecular mechanisms that are involved in this detrimental process. Fuller understanding of this complex mechanism may lead to the development of improved therapeutics meant to interrupt the pathologic effects of excess iron on bone.
病因多样的疾病/病症，如血红蛋白病、遗传性血色素沉着症和更年期，可能导致慢性铁蓄积。这种情况常与一种骨表型相关；其特征为骨量低、骨质疏松/骨量减少、微观结构和生物力学改变，以及骨折发生率增加。骨质疏松性骨表型是铁过载患者的主要并发症。本综述的目的是总结我们从临床研究和动物模型中了解到的关于铁过载相关骨质流失的情况。骨是一种代谢活跃的组织，在破骨细胞吸收矿化骨和成骨细胞形成新骨的参与下不断进行重塑。越来越多的证据表明，在铁过载情况下，骨吸收增加和骨形成减少均参与了病理性骨质流失。我们将讨论参与这一有害过程的细胞和分子机制。对这一复杂机制的更全面理解可能会促使开发出改进的治疗方法，以阻断过量铁对骨的病理作用。
