Iron Metabolism in Aging and Age-Related Diseases

Tian, Yao; Tian, Yuanliangzi; Yuan, Zhixiao; Zeng, Yutian; Wang, Shuai; Fan, Xiaolan; Yang, Deying; Yang, Mingyao

doi:10.3390/ijms23073612

Cited by 42 publications

(33 citation statements)

References 155 publications

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“…It has been reported that the translation of the APP is regulated by cellular iron levels (Peng et al, 2021). α-secretase and β-secretase activation is particularly critical to attenuate or increase the formation of Aβ and its accumulation in the brain (Tian et al, 2022). The process is regulated by furin, whose transcription is regulated by intracellular iron concentration.…”

Section: Iron Metabolism and Alzheimer's Diseasementioning

confidence: 99%

The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism

Long

Zhou

Cheng

et al. 2022

Front. Aging Neurosci.

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Alzheimer’s disease (AD), the most common type of senile dementia, includes the complex pathogenesis of abnormal deposition of amyloid beta-protein (Aβ), phosphorylated tau (p-tau) and neuroimmune inflammatory. The neurodegenerative process of AD triggers microglial activation, and the overactivation of microglia produces a large number of neuroimmune inflammatory factors. Microglia dysfunction can lead to disturbances in iron metabolism and enhance iron-induced neuronal degeneration in AD, while elevated iron levels in brain areas affect microglia phenotype and function. In this manuscript, we firstly discuss the role of microglia in AD and then introduce the role of microglia in the immune-inflammatory pathology of AD. Their role in AD iron homeostasis is emphasized. Recent studies on microglia and ferroptosis in AD are also reviewed. It will help readers better understand the role of microglia in iron metabolism in AD, and provides a basis for better regulation of iron metabolism disorders in AD and the discovery of new potential therapeutic targets for AD.

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Section: Iron Metabolism and Alzheimer's Diseasementioning

confidence: 99%

The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism

Long

Zhou

Cheng

et al. 2022

Front. Aging Neurosci.

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“…The mobilization of intracellular labile iron pools is one of the major determinants of ferroptosis. 7,[41][42][43] Ferritin can protect cells from ironinduced oxidative stress by buffering LIP. However, iron sequestered in the ferritin shells may become prooxidant in a chronic overexpression process of ferritin and finally lead to ferroptotic cell death.…”

Section: Discussionmentioning

confidence: 99%

“…The iron‐containing transferrin binds to transferrin receptor 1 on the membrane of the cell and is then internalized via endocytosis. The mobilization of intracellular labile iron pools is one of the major determinants of ferroptosis 7,41–43 . Ferritin can protect cells from iron‐induced oxidative stress by buffering LIP.…”

Section: Discussionmentioning

confidence: 99%

Iron overload‐induced ferroptosis of osteoblasts inhibits osteogenesis and promotes osteoporosis: An in vitro and in vivo study

Jiang

Wang

et al. 2022

IUBMB Life

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Growing evidence indicates that iron overload is an independent risk factor for osteoporosis. However, the mechanisms are not fully understood. The purpose of our study was to determine whether iron overload could lead to ferroptosis in osteoblasts and to explore whether ferroptosis of osteoblasts is involved in iron overload‐induced osteoporosis in vitro and in vivo. Ferric ammonium citrate was used to mimic iron overload conditions, while deferoxamine and ferrostatin‐1 were used to inhibit ferroptosis of MC3T3‐E1 cells in vitro. The ferroptosis, osteogenic differentiation and mineralization of MC3T3‐E1 cells were assessed in vitro. A mouse iron overload model was established using iron dextran. Immunohistochemical analysis was performed to determine ferroptosis of osteoblasts in vivo. Enzyme‐linked immunosorbent assays and calcein–alizarin red S labelling were used to assess new bone formation. Dual x‐ray absorptiometry, micro‐computed tomography and histopathological analysis were conducted to evaluate osteoporosis. The results showed that iron overload reduced cell viability, superoxide dismutase and glutathione levels, increased reactive oxygen species generation, lipid peroxidation, malondialdehyde levels and ferroptosis‐related protein expression, and induced ultrastructural changes in mitochondria. Iron overload could also inhibit osteogenic differentiation and mineralization in vitro. Inhibiting ferroptosis reversed the changes described above. Iron overload inhibited osteogenesis, promoted the ferroptosis of osteoblasts and induced osteoporosis in vivo, which could also be improved by deferoxamine and ferrostatin‐1. These results demonstrate that ferroptosis of osteoblasts plays a crucial role in iron overload‐induced osteoporosis. Maintaining iron homeostasis and targeting ferroptosis of osteoblasts might be potential measures of treating or preventing iron overload‐induced osteoporosis.

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“…These inconsistent results could reflect different responses of ferritin production under different illness states and at different ages since serum ferritin (47,52) and brain iron and ferritin content increase with aging (53)(54)(55)(56)(57), rendering elderly patients with psychiatric disorders vulnerable to oxidative damage (58), ferroptosis (59) and mortality (60) during severe COVID- 19.…”

Section: Introductionmentioning

confidence: 99%

Attenuated initial serum ferritin concentration in critically ill coronavirus disease 2019 geriatric patients with comorbid psychiatric conditions

Abulseoud

Yehia²,

Egol³

et al. 2022

Front. Psychiatry

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We examined the effects of psychiatric comorbidity, sex, and ICU admission on serum ferritin concentration in 628 elderly patients (79.7 ± 8.5 years) with positive SARS-CoV-2 PCR test. Hospitalization was required in 96% of patients and 17% required ICU admission. Patients with COVID-19 and psychiatric comorbidities (n = 212) compared to patients without psychiatric comorbidities (n = 416) had significantly lower ferritin concentration (570.4 ± 900.1 vs. 744.1 ± 965, P = 0.029), a greater incidence of delirium (22.6 vs. 14.4%, P = 0.013) and higher mortality (35.3 vs. 27.6%, P = 0.015). Furthermore, we found significant effects for sex (P = 0.002) and ICU admission (P = 0.007). Among patients without comorbid psychiatric conditions, males had significantly higher ferritin compared to females (1,098.3 ± 78.4 vs. 651.5 ± 94.4, P < 0.001). ICU patients without comorbid psychiatric conditions had significantly higher serum ferritin compared to ICU patients with comorbid psychiatric conditions: (1,126.6 ± 110.7 vs. 668.6 ± 156.5, P < 0.001). Our results suggest that the presence of comorbid psychiatric conditions in elderly patients with COVID-19 is associated with higher rates of delirium and mortality and lower ferritin levels during severe illness. Whether high serum ferritin is protective during severe infection requires further investigation.

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Iron Metabolism in Aging and Age-Related Diseases

Cited by 42 publications

References 155 publications

The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism

The Role of Microglia in Alzheimer’s Disease From the Perspective of Immune Inflammation and Iron Metabolism

Iron overload‐induced ferroptosis of osteoblasts inhibits osteogenesis and promotes osteoporosis: An in vitro and in vivo study

Attenuated initial serum ferritin concentration in critically ill coronavirus disease 2019 geriatric patients with comorbid psychiatric conditions

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