The Effect of Abnormal Iron Metabolism on Osteoporosis

Che, Jingmin; Yang, Juhua; Zhao, Bin; Zhang, Ge; Wang, Luyao; Peng, Songlin; Shang, Peng

doi:10.1007/s12011-019-01867-4

Cited by 68 publications

(40 citation statements)

References 150 publications

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“…An association between excess iron and osteoporosis as well as fracture has been shown which is attributed to the detrimental effect of iron on bone. Iron overload decreases osteoplastic activity and facilitates osteoplastic differentiation and bone resorption; furthermore, iron inhibits differentiation of bone marrow mesenchymal cells and bone remodeling, through induction of ferritin [21,22]. FAC, respectively.…”

Section: Discussionmentioning

confidence: 99%

Iron-Chelating Agent Can Maintain Bone Homeostasis Disrupted by Iron Overload by Upregulating Wnt/Beta-Catenin Signaling

Zhu

et al. 2020

BioMed Research International

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Background. The incidence of osteoporotic fractures is increasing. In this study, we explored the activities of Wnt/β-catenin signaling in bone tissues with iron accumulation. Methods. We established rat bipedal walking models (RBWM), and a portion of our RBWM rats were intraperitoneally injected with ferric ammonium citrate, normal saline, and deferoxamine. Bone mineral density was measured with a small animal in vivo imaging system. The protein levels of ferritin, TRAP-5B, RANKL, and OPG in serum were measured by the enzyme-linked immunosorbent assay (ELISA). Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to quantify the RNA and protein expression levels of certain regulators involved in Wnt/β-catenin signaling in bone tissues. Results. In the present study, we established a rat bipedal walking model containing 32 bipedal rats, which were randomly classified into four groups, termed as NS, FAC, FAC+NS, and FAC+DFO. Those three experimental groups with FAC injection had significantly lower bone mineral density (BMD) than the control group NS (P<0.05). The disruption of bone homeostasis and downregulation of Wnt/β-catenin signaling were also observed in the three groups with FAC injection. Moreover, after the injection of deferoxamine, those aberrations in samples with FAC injection seemed repaired as test results returning or getting close to normal ranges. Conclusion. The osteoporosis could be caused by iron overload, which reduced the bone mineral density by disrupting the homeostasis of bone formation and absorption and attenuating the Wnt/β-catenin signaling in bone tissues. The deferoxamine had the potential to improve the bone health by reducing the accumulation of iron and increasing the bone mass, which might be a promising therapeutic solution for osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Iron-Chelating Agent Can Maintain Bone Homeostasis Disrupted by Iron Overload by Upregulating Wnt/Beta-Catenin Signaling

Zhu

et al. 2020

BioMed Research International

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“…What merits attention is that the endothelial cell-secreted exosome has proven to throw a wrench in the glucocorticoid-induced osteoporosis process by abating ferritinophagy (Yang et al, 2021). Dysregulation of iron homeostasis and metabolism is substantiated to have a close connection to diverse metabolic diseases, such as diabetes (Dubey et al, 2020), obesity, metabolic syndrome (Gonzalez-Dominguez et al, 2020), osteoporosis (Che et al, 2020;Sato et al, 2020) and AS (Wunderer et al, 2020). Thereby, we forecast that the link between exosome and iron metastasis in ferroptosis may be a heated discussion in the near future.…”

Section: Labile Iron Pool-powerful Strength Of the Elder Wandmentioning

confidence: 99%

“…Accumulating researches have demonstrated that inordinate iron metabolism can destroy bone homeostasis inducing osteoporosis, which is a systemic metabolic disease characterized by reduced bone mass, augmented bone fragility and increased risk of fracture (Che et al, 2020). Conducted within certain iron overload models, the phenotype of diminished bone density and trabecular thickness was observed due to heightened osteoclast differentiation and osteoblast apoptosis, leading to intense bone dissolution and abating bone formation due to decreased osteoblast specific genes, i.e., alkaline phosphatase (ALP), runtrelated transcription factor 2 (Runx2) and type I collagen (Tsay et al, 2010;Li et al, 2012;Chen et al, 2014;Cheng et al, 2017).…”

Section: Ferroptosis and Osteoporosismentioning

confidence: 99%

“…Conducted within certain iron overload models, the phenotype of diminished bone density and trabecular thickness was observed due to heightened osteoclast differentiation and osteoblast apoptosis, leading to intense bone dissolution and abating bone formation due to decreased osteoblast specific genes, i.e., alkaline phosphatase (ALP), runtrelated transcription factor 2 (Runx2) and type I collagen (Tsay et al, 2010;Li et al, 2012;Chen et al, 2014;Cheng et al, 2017). Redundant iron stimulates osteoclasts and osteoblasts to yield a generous amount of ROS, engendering maladjustment of the intracellular antioxidant/peroxidation balance system by activating the MAPKs and NF-κB pathways, resulting in osteoblast death (Ray et al, 2012;Che et al, 2020). All of the above discoveries foreshadow that ferroptosis may participate in the development of osteoporosis, especially the devitalization of osteoblasts.…”

Section: Ferroptosis and Osteoporosismentioning

confidence: 99%

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Ferroptosis and Its Potential Role in Metabolic Diseases: A Curse or Revitalization?

Duan

Lin

et al. 2021

Front. Cell Dev. Biol.

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Ferroptosis is classified as an iron-dependent form of regulated cell death (RCD) attributed to the accumulation of lipid hydroperoxides and redox imbalance. In recent years, accumulating researches have suggested that ferroptosis may play a vital role in the development of diverse metabolic diseases, for example, diabetes and its complications (e.g., diabetic nephropathy, diabetic cardiomyopathy, diabetic myocardial ischemia/reperfusion injury and atherosclerosis [AS]), metabolic bone disease and adrenal injury. However, the specific physiopathological mechanism and precise therapeutic effect is still not clear. In this review, we summarized recent advances about the development of ferroptosis, focused on its potential character as the therapeutic target in metabolic diseases, and put forward our insights on this topic, largely to offer some help to forecast further directions.

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“…For example, baicalein subcutaneously applications improved the cortical bone parameters in ovariectomized rats [136]. Nevertheless, iron deficiency and excess can be high risk factors for the osteoporosis, both of them can lead to bone loss [137,138]. Excess of iron stimulate degradation of bone matrix (type I collagen) and triggers severe inflammatory reactions [139].…”

Section: Future Directionmentioning

confidence: 99%

Iron Complexes of Flavonoids-Antioxidant Capacity and Beyond

Kejík

Kaplánek

Masařík

et al. 2021

IJMS

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Flavonoids are common plant natural products able to suppress ROS-related damage and alleviate oxidative stress. One of key mechanisms, involved in this phenomenon is chelation of transition metal ions. From a physiological perspective, iron is the most significant transition metal, because of its abundance in living organisms and ubiquitous involvement in redox processes. The chemical, pharmaceutical, and biological properties of flavonoids can be significantly affected by their interaction with transition metal ions, mainly iron. In this review, we explain the interaction of various flavonoid structures with Fe(II) and Fe(III) ions and critically discuss the influence of chelated ions on the flavonoid biochemical properties. In addition, specific biological effects of their iron metallocomplexes, such as the inhibition of iron-containing enzymes, have been included in this review.

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The Effect of Abnormal Iron Metabolism on Osteoporosis

Cited by 68 publications

References 150 publications

Iron-Chelating Agent Can Maintain Bone Homeostasis Disrupted by Iron Overload by Upregulating Wnt/Beta-Catenin Signaling

Iron-Chelating Agent Can Maintain Bone Homeostasis Disrupted by Iron Overload by Upregulating Wnt/Beta-Catenin Signaling

Ferroptosis and Its Potential Role in Metabolic Diseases: A Curse or Revitalization?

Iron Complexes of Flavonoids-Antioxidant Capacity and Beyond

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