Clinical impact and cellular mechanisms of iron overload-associated bone loss

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Article number77
JournalFrontiers in Pharmacology
Volume8
Issue numberFEB
DOIs
Publication statusPublished - Feb 21 2017

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Iron Overload
Bone and Bones
Iron
Phenotype
Hemoglobinopathies
Hemochromatosis
Metabolic Bone Diseases
Osteoclasts
Bone Resorption
Menopause
Osteoblasts
Biomechanical Phenomena
Osteogenesis
Osteoporosis
Animal Models
Incidence

Keywords

  • Iron overload disease
  • Osteoblast differentiation
  • Osteoclasts
  • Osteoporosis
  • RUNX2

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Cite this

Clinical impact and cellular mechanisms of iron overload-associated bone loss. / Jeney, V.

In: Frontiers in Pharmacology, Vol. 8, No. FEB, 77, 21.02.2017.

Research output: Contribution to journalArticle

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