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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: 31 October 2024 | Viewed by 2129

Special Issue Editors


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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

Published Papers (2 papers)

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Review

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
Viewed by 961
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
Viewed by 885
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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