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Iron Dyshomeostasis
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Iron Dyshomeostasis

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

Deadline for manuscript submissions: closed (20 February 2025) | Viewed by 5013

Special Issue Editors

Dr. Carlo Marya Thomas Marobbio

E-Mail Website
Guest Editor
Department of Biosciences, Biotechnology and Environment, University of Bari, Via Orabona 4, 70125 Bari, Italy
Interests: mitochondrial diseases; mitochondrial transport proteins; mitochondrial metabolism; oxidative stress; iron metabolism; iron dyshomeostasis
Dr. Sara Anjomani Virmouni

E-Mail Website
Guest Editor
Department of Life Sciences, Brunel University London, London, UK
Interests: neurodegeneration; Friedreich’s ataxia; metabolomics; mouse models; oxidative stress; mitochondrial function

Special Issue Information

Dear Colleagues, 

Iron plays a crucial role in many physiological processes of the human body. A plethora of highly conserved regulatory and signaling pathways comprising metal uptake, transport, release, cellular storage, and metal recycling tightly control the dynamics of iron distribution inside the cells. Iron dyshomeostasis is usually associated with altered distribution and accumulation of iron in different compartments of cells. It is connected to multifactorial cellular dysfunction, causing oxidative stress, iron-induced lipid peroxidation, inflammatory responses, and ferroptosis, a programmed cell death process associated with iron dysregulation. It is supposed to be linked to many pathological processes, especially blood disorders, cancer, metabolic disorders, neurodegenerative diseases, as well as viral infections. In this collection, we will present an updated view of iron dyshomeostasis, discussing the associations with pathological processes. It will be also discussed how accumulated knowledge on this process is helping the creation of novel therapeutic strategies.

Dr. Carlo Marya Thomas Marobbio
Dr. Sara Anjomani Virmouni
Guest Editors

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Keywords

  • iron metabolism

  • iron dyshomeostasis
  • ferroptosis
  • oxidative stress
  • mitochondrial disease

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Published Papers (3 papers)

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Research

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13 pages, 1705 KiB  
Article
P2 Receptor Antagonists Rescue Defective Heme Content in an In Vitro SLC25A38-Associated Congenital Sideroblastic Anemia Cell Model
by Antonella Santoro, Silvia De Santis, Ferdinando Palmieri, Angelo Vozza, Gennaro Agrimi, Immacolata Andolfo, Roberta Russo, Antonio Palazzo, Clelia Tiziana Storlazzi, Arianna Ferrucci, Yong Woong Jun, Eric T. Kool, Giuseppe Fiermonte, Achille Iolascon, Eleonora Paradies, Carlo Marya Thomas Marobbio and Luigi Palmieri
Int. J. Mol. Sci. 2024, 25(24), 13314; https://doi.org/10.3390/ijms252413314 - 12 Dec 2024
Viewed by 1058
Abstract
Mutations in the SLC25A38 gene are responsible for the second most common form of congenital sideroblastic anemia (CSA), a severe condition for which no effective treatment exists. We developed and characterized a K562 erythroleukemia cell line with markedly reduced expression of the SLC25A38 [...] Read more.
Mutations in the SLC25A38 gene are responsible for the second most common form of congenital sideroblastic anemia (CSA), a severe condition for which no effective treatment exists. We developed and characterized a K562 erythroleukemia cell line with markedly reduced expression of the SLC25A38 protein (A38-low cells). This model successfully recapitulated the main features of CSA, including reduced heme content and mitochondrial respiration, increase in mitochondrial iron, ROS levels and sensitivity to oxidative stress. Notably, our study uncovered a new role for extracellular pyridoxal 5′-phosphate (PLP) and other P2 receptor antagonists in rescuing the altered parameters of A38-low cells (for example, the heme content of the A38-low cells was increased from about 50% to about 80% by the P2 receptor antagonists treatment compared with the value of the controls). These findings suggest that targeting P2 receptors could represent a promising therapeutic approach for SLC25A38-associated CSA. Full article
(This article belongs to the Special Issue Iron Dyshomeostasis)
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Review

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14 pages, 2208 KiB  
Review
The Relationship Between Non-Transferrin-Bound Iron (NTBI), Labile Plasma Iron (LPI), and Iron Toxicity
by Lorena Duca, Elena Di Pierro, Natalia Scaramellini, Francesca Granata and Giovanna Graziadei
Int. J. Mol. Sci. 2025, 26(13), 6433; https://doi.org/10.3390/ijms26136433 - 3 Jul 2025
Viewed by 207
Abstract
Plasma non-transferrin-bound iron (NTBI) comprises multiple subspecies, classified by their composition, chemical reactivity, and susceptibility to chelation. The redox-active and chelatable fraction of NTBI is referred to as labile plasma iron (LPI). The pathophysiological significance of NTBI and LPI lies in their ability [...] Read more.
Plasma non-transferrin-bound iron (NTBI) comprises multiple subspecies, classified by their composition, chemical reactivity, and susceptibility to chelation. The redox-active and chelatable fraction of NTBI is referred to as labile plasma iron (LPI). The pathophysiological significance of NTBI and LPI lies in their ability to enter cells via alternative transport pathways that are not regulated by the transferrin receptor system or by cellular iron levels. Several mechanisms have been proposed for their cellular entry, including the hijacking of divalent metal transporters and passive diffusion. This unregulated uptake can lead to iron accumulation in vulnerable tissues such as the liver and the heart. NTBI and LPI bypassing normal cellular control mechanisms can rapidly exceed the cell’s capacity to safely store excess iron, leading to toxicity. Both NTBI and LPI contribute to oxidative stress by participating in free-radical-generating reactions. However, LPI concentration in the bloodstream may be differentially affected by the mode and extent of iron overload, the presence of residual serum iron-binding activity, and the antioxidant capacity of individual sera. In summary, both NTBI and LPI contribute to iron-mediated toxicity but differ in terms of reactivity, availability, and pathogenic potential depending on the pathophysiological conditions that influence the degree of toxicity. Full article
(This article belongs to the Special Issue Iron Dyshomeostasis)
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17 pages, 1222 KiB  
Review
The Role of Cellular Defense Systems of Ferroptosis in Parkinson’s Disease and Alzheimer’s Disease
by Jie Chu, Jingwen Li, Lin Sun and Jianshe Wei
Int. J. Mol. Sci. 2023, 24(18), 14108; https://doi.org/10.3390/ijms241814108 - 14 Sep 2023
Cited by 10 | Viewed by 2790
Abstract
Parkinson’s disease (PD) and Alzheimer’s disease (AD) are the most common rapidly developing neurodegenerative diseases that lead to serious health and socio-economic consequences. Ferroptosis is a non-apoptotic form of cell death; there is growing evidence to support the notion that ferroptosis is involved [...] Read more.
Parkinson’s disease (PD) and Alzheimer’s disease (AD) are the most common rapidly developing neurodegenerative diseases that lead to serious health and socio-economic consequences. Ferroptosis is a non-apoptotic form of cell death; there is growing evidence to support the notion that ferroptosis is involved in a variety of pathophysiological contexts, and there is increasing interest in the role of ferroptosis in PD and AD. Simultaneously, cells may have evolved four defense systems to counteract the toxic effects of ferroptosis occasioned by lipid peroxidation. This review, which focuses on the analysis of ferroptosis in the PD and AD context, outlines four cellular defense systems against ferroptosis and how each of them is involved in PD and AD. Full article
(This article belongs to the Special Issue Iron Dyshomeostasis)
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