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Editorial Board Members’ Collection Series: Iron Homeostasis
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Editorial Board Members’ Collection Series: Iron Homeostasis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 5791

Special Issue Editors

Prof. Dr. Paolo Arosio

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy
Interests: iron metabolism; ferritin; iron storage
Special Issues, Collections and Topics in MDPI journals
Dr. Antonella Roetto

E-Mail Website
Guest Editor
Department of Clinical & Biological Science, University of Torino, I-1043 Orbassano, Italy
Interests: free radical biology; cancer; oxidative stress; iron

Special Issue Information

Dear Colleagues,

Iron is essential for almost all living organisms since it is involved in critical biochemical processes such as the transport of oxygen, respiration, synthesis and repair of DNA, amongst others. However, iron is also potentially toxic when in excess or deregulated, and its dysregulation can lead to severe health consequences. The dynamic equilibrium of iron homeostasis within the body is governed by a complex regulated interplay of absorption, transport, utilization, and storage mechanisms. Thus, iron metabolism involves the study of its absorption, transport, utilization, storage, emerging roles of iron in inflammation, cellular signaling, and the relationship with the microbiome. It includes iron overload and iron-deficient diseases and examination to develop new and efficient therapies. Of importance, iron is involved in ferroptosis, a non-apoptotic programmed death mechanism that plays a role In cancer, neurodegeneration, and various other pathologies. This special Issue aims to present the latest research or new views on human iron metabolism, and original research articles and comprehensive reviews are welcomed.

Prof. Dr. Paolo Arosio
Dr. Antonella Roetto
Guest Editors

Manuscript Submission Information

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Keywords

  • iron metabolism
  • iron homeostasis
  • iron-deficient diseases
  • iron overload
  • ferroptosis

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Published Papers (4 papers)

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Research

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15 pages, 3409 KiB  
Article
Lack of Hfe and TfR2 in Macrophages Impairs Iron Metabolism in the Spleen and the Bone Marrow
by Stefano Comità, Patrizia Falco, Mariarosa Mezzanotte, Maja Vujić Spasić and Antonella Roetto
Int. J. Mol. Sci. 2024, 25(17), 9142; https://doi.org/10.3390/ijms25179142 - 23 Aug 2024
Viewed by 706
Abstract
Iron is a vital element involved in a plethora of metabolic activities. Mammalian systemic iron homeostasis is mainly modulated by hepcidin, the synthesis of which is regulated by a number of proteins, including the hemochromatosis-associated proteins Hfe and Transferrin Receptor 2 (TfR2). Macrophages [...] Read more.
Iron is a vital element involved in a plethora of metabolic activities. Mammalian systemic iron homeostasis is mainly modulated by hepcidin, the synthesis of which is regulated by a number of proteins, including the hemochromatosis-associated proteins Hfe and Transferrin Receptor 2 (TfR2). Macrophages play versatile functions in iron homeostasis by storing iron derived from the catabolism of erythrocytes and supplying iron required for erythropoiesis. The absence of Hfe in macrophages causes a mild iron deficiency in aged mice and leads to an overproduction of the iron exporter Ferroportin 1 (Fpn1). Conversely, TfR2 gene silencing in macrophages does not influence systemic iron metabolism but decreases transcription of the macrophage Fpn1 in adult mice and modulates their immune response. This study investigated cellular and systemic iron metabolism in adult and aged male mice with macrophage-specific Hfe and TfR2 silencing (double knock-out, DKO). Serum iron parameters were significantly modified in aged animals, and significant differences were found in hepatic hepcidin transcription at both ages. Interestingly, splenic iron content was low in adult DKOs and splenic Fpn1 transcription was significantly increased in DKO animals at both ages, while the protein amount does not reflect the transcriptional trend. Additionally, DKO macrophages were isolated from mice bone marrow (BMDMs) and showed significant variations in the transcription of iron genes and protein amounts in targeted mice compared to controls. Specifically, Tranferrin Receptor 1 (TfR1) increased in DKO adult mice BMDMs, while the opposite is observed in the cells of aged DKO mice. Fpn1 transcript was significantly decreased in the BMDMs of adult DKO mice, while the protein was reduced at both ages. Lastly, a significant increase in Erythropoietin production was evidenced in aged DKO mice. Overall, our study reveals that Hfe and TfR2 in macrophages regulate hepatic Hepc production and affect iron homeostasis in the spleen and BMDMs, leading to an iron deficiency in aged animals that impairs their erythropoiesis. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Iron Homeostasis)
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21 pages, 2946 KiB  
Article
Infection vs. Reinfection: The Immunomodulation of Erythropoiesis
by Ana Catarina Pêgo, Illyane Sofia Lima, Ana Catarina Martins, Inês Sá-Pereira, Gracelino Martins and Raffaella Gozzelino
Int. J. Mol. Sci. 2024, 25(11), 6153; https://doi.org/10.3390/ijms25116153 - 3 Jun 2024
Viewed by 681
Abstract
Severe malarial anemia (SMA) increases the morbidity and mortality of Plasmodium, the causative agent of malaria. SMA is mainly developed by children and pregnant women in response to the infection. It is characterized by ineffective erythropoiesis caused by impaired erythropoietin (EPO) signaling. [...] Read more.
Severe malarial anemia (SMA) increases the morbidity and mortality of Plasmodium, the causative agent of malaria. SMA is mainly developed by children and pregnant women in response to the infection. It is characterized by ineffective erythropoiesis caused by impaired erythropoietin (EPO) signaling. To gain new insights into the pathogenesis of SMA, we investigated the relationship between the immune system and erythropoiesis, conducting comparative analyses in a mouse model of malaria. Red blood cell (RBC) production was evaluated in infected and reinfected animals to mimic endemic occurrences. Higher levels of circulating EPO were observed in response to (re)infection. Despite no major differences in bone marrow erythropoiesis, compensatory mechanisms of splenic RBC production were significantly reduced in reinfected mice. Concomitantly, a pronounced immune response activation was observed in erythropoietic organs of reinfected animals in relation to single-infected mice. Aged mice were also used to mimic the occurrence of malaria in the elderly. The increase in symptom severity was correlated with the enhanced activation of the immune system, which significantly impaired erythropoiesis. Immunocompromised mice further support the existence of an immune-shaping regulation of RBC production. Overall, our data reveal the strict correlation between erythropoiesis and immune cells, which ultimately dictates the severity of SMA. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Iron Homeostasis)
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Review

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14 pages, 1019 KiB  
Review
Iron Supplementation of Pregnant Sows to Prevent Iron Deficiency Anemia in Piglets: A Procedure of Questionable Effectiveness
by Rafał Mazgaj, Paweł Lipiński and Rafał R. Starzyński
Int. J. Mol. Sci. 2024, 25(7), 4106; https://doi.org/10.3390/ijms25074106 - 8 Apr 2024
Cited by 1 | Viewed by 2175
Abstract
In pigs, iron deficiency anemia (IDA) is a common disorder that occurs during the early postnatal period, leading to the stunted growth and increased mortality of piglets. The main cause of IDA is low iron stores in the liver of newborn piglets; these [...] Read more.
In pigs, iron deficiency anemia (IDA) is a common disorder that occurs during the early postnatal period, leading to the stunted growth and increased mortality of piglets. The main cause of IDA is low iron stores in the liver of newborn piglets; these stores constitute the main source of iron needed to satisfy the erythropoietic requirements of the piglets in their first weeks of life. Insufficient iron stores in piglets are usually due to the inadequate placental iron transfer from the sow to the fetuses. Therefore, iron supplementation in pregnant sows has been implemented to enhance placental iron transfer and increase iron accumulation in the liver of the fetuses. Over the years, several oral and parenteral approaches have been attempted to supplement sows with various iron preparations, and consequently, to improve piglets’ red blood cell indices. However, there is debate with regard to the effectiveness of iron supplementation in pregnant sows for preventing IDA in newborn piglets. Importantly, this procedure should be carried out with caution to avoid iron over-supplementation, which can lead to iron toxicity. This article aims to critically review and evaluate the use of iron supplementation in pregnant sows as a procedure for preventing IDA in piglets. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Iron Homeostasis)
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25 pages, 1175 KiB  
Review
HFE Mutations in Neurodegenerative Disease as a Model of Hormesis
by Savannah L. Marshall Moscon and James R. Connor
Int. J. Mol. Sci. 2024, 25(6), 3334; https://doi.org/10.3390/ijms25063334 - 15 Mar 2024
Cited by 3 | Viewed by 1723
Abstract
Common variants in the iron regulatory protein HFE contribute to systematically increased iron levels, yet the effects in the brain are not fully characterized. It is commonly believed that iron dysregulation is a key contributor to neurodegenerative disease due to iron’s ability to [...] Read more.
Common variants in the iron regulatory protein HFE contribute to systematically increased iron levels, yet the effects in the brain are not fully characterized. It is commonly believed that iron dysregulation is a key contributor to neurodegenerative disease due to iron’s ability to catalyze reactive oxygen species production. However, whether HFE variants exacerbate or protect against neurodegeneration has been heavily debated. Some claim that mutated HFE exacerbates oxidative stress and neuroinflammation, thus predisposing carriers to neurodegeneration-linked pathologies. However, H63D HFE has also been shown to slow the progression of multiple neurodegenerative diseases and to protect against environmental toxins that cause neurodegeneration. These conflicting results showcase the need to further understand the contribution of HFE variants to neurodegenerative disease heterogeneity. Data from mouse models consistently demonstrate robust neuroprotection against toxins known to increase the risk of neurodegenerative disease. This may represent an adaptive, or hormetic, response to increased iron, which leaves cells better protected against future stressors. This review describes the current research regarding the contribution of HFE variants to neurodegenerative disease prognosis in the context of a hormetic model. To our knowledge, this is the first time that a hormetic model for neurodegenerative disease has been presented. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Iron Homeostasis)
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