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Biomolecules
Special Issues
Iron Metabolism in Cells
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Iron Metabolism in Cells

A Special Issue of Biomolecules (ISSN 2218-273X) belonging to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 6692

Editors

Dr. Magdalena Gryzik

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, 25121 Brescia, Italy
Interests: iron metabolism; ferritinophagy; ferritin; ferroptosis; tumor
Dr. Michela Asperti

E-Mail Website
Guest Editor
Department of Theoretical and Applied Sciences, eCampus University, Novedrate, 22060 Como, Italy
Interests: iron metabolism; hepcidin regulation; heparan sulfate; heparin; ferroptosis; tumor
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Iron is an essential micronutrient for various biological processes, but it can be toxic when participating in the Fenton reaction and thus contributing to the production of reactive oxygen species (ROS). It is important to maintain cellular iron homeostasis by regulating its uptake, storage, utilization, and exportation. Alterations to any iron-related pathway may lead to iron dysregulation, depletion, or overload, associated with disorders such as anemia or hemochromatosis. Iron can also contribute to tumorigenesis, and ‘iron addiction’ is a well-described phenomenon in cancer cells. Recently, other diseases, such as neurodegenerative disorders, have been linked to altered iron metabolism and the occurrence of iron-dependent cell death, ferroptosis. Overall, growing interest in iron’s involvement in biological and pathological processes has led to new directions in in vitro studies, allowing us to better understand the molecular basis behind these processes.

We are pleased to invite you to contribute to this Special Issue of Biomolecules, titled ‘Iron Metabolism in Cells’. This Special Issue aims to provide an overview of recent research on cellular iron metabolism, including biological processes such as iron transport and utilization and their regulation in physiological and pathological conditions, along with potential therapeutic applications.

For this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) biochemistry, molecular biology, pharmacology, cell biology, and molecular medicine.

We look forward to receiving your contributions.

Dr. Magdalena Gryzik
Dr. Michela Asperti
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • iron metabolism
  • iron-related proteins
  • iron uptake
  • iron storage
  • mitochondrial iron metabolism
  • iron sensing mechanism
  • ferroptosis

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Published Papers (5 papers)

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Research

Jump to: Review

20 pages, 4955 KB  
Article
Role of Endogenous Myoglobin in Anthracycline Response in Breast Cancer
by Ilona Rybinska, Andreas Petry, Thomas Hankeln, Thomas A. Gorr and Gaetano Cairo
Biomolecules 2026, 16(7), 1055; https://doi.org/10.3390/biom16071055 - 18 Jul 2026
Viewed by 494
Abstract
Anthracyclines such as doxorubicin (DOX) remain central components of breast cancer (BC) chemotherapy, although their efficacy is frequently limited by drug resistance. Myoglobin (MB), an oxygen-binding heme protein expressed in breast tumors, has been implicated in the detoxification of DOX in cardiomyocytes, but [...] Read more.
Anthracyclines such as doxorubicin (DOX) remain central components of breast cancer (BC) chemotherapy, although their efficacy is frequently limited by drug resistance. Myoglobin (MB), an oxygen-binding heme protein expressed in breast tumors, has been implicated in the detoxification of DOX in cardiomyocytes, but its role in BC remains unclear. Using MB-expressing and MB-knockout (MBKO) MDA-MB-468 BC cells, we demonstrate that MB confers hypoxia-dependent resistance to DOX. Under hypoxia, MB-expressing cells exhibited reduced intracellular DOX-associated fluorescence, enhanced superoxide generation, and decreased sensitivity to DOX, findings consistent with altered redox cycling and oxidative processing of the drug. Re-expression of MB in MBKO cells restored resistance, whereas pharmacological modulation of MB function using carbon monoxide-releasing molecule-3 and tert-butoxycarbonyl-alanine reversed MB-dependent reductions in intracellular DOX accumulation. In contrast, aclarubicin, an anthracycline lacking the hydroquinone moiety required for efficient redox cycling, failed to reproduce MB-dependent effects. Analyses of four independent neoadjuvant BC cohorts further demonstrated that elevated MB expression was consistently associated with reduced probability of achieving pathological complete response following anthracycline-containing chemotherapy. Collectively, these findings identify MB as a previously unrecognized modulator of BC response to redox-active anthracyclines and support its potential utility as both a predictive biomarker and therapeutic target. Full article
(This article belongs to the Special Issue Iron Metabolism in Cells)
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11 pages, 952 KB  
Article
Beyond Iron Solubility: Particle Size as a Determinant of Cell Survival and Iron-Induced COX-2 Expression in Human Intestinal Cells
by Agata Tarczykowska, Amir Saeid Mohammadi and Nathalie Scheers
Biomolecules 2026, 16(3), 388; https://doi.org/10.3390/biom16030388 - 5 Mar 2026
Viewed by 786
Abstract
Background: Oral iron supplementation or food fortification is essential for managing or preventing iron deficiency but often causes gastrointestinal side effects. While solubility has traditionally been considered a requirement for iron uptake via the DMT1 transporter, recent evidence shows that insoluble iron can [...] Read more.
Background: Oral iron supplementation or food fortification is essential for managing or preventing iron deficiency but often causes gastrointestinal side effects. While solubility has traditionally been considered a requirement for iron uptake via the DMT1 transporter, recent evidence shows that insoluble iron can also be absorbed through endocytosis, raising questions about particle size and epithelial responses. Methods: Human intestinal cell lines (Hutu-80 and Caco-2) were exposed to physiologically relevant but elevated iron levels (0.5 mM Fe, 48 h) as ferric pyrophosphate, ferrous fumarate (both prone to precipitation), and soluble ferric EDTA. Cell survival and COX-2 protein were quantified by ELISA, solubility by ICP-OES, and particle size in cell culture medium by dynamic light scattering analyses. Results: Ferric pyrophosphate (0.62–3.8 μm) markedly increased COX-2 expression in Hutu-80 cells (254% ± 37%, n = 3, p = 4.11 × 10−5) and in Caco-2 cells (78% ± 8%, n = 3, p = 0.01) compared to the control. Ferrous fumarate (237–866 nm) also induced COX-2, but only in Hutu-80 cells (62% ± 11%, n = 3, p = 0.04), whereas ferric EDTA showed no effect in either cell line. COX-2 induction was associated with larger particles in the medium (≥237 nm), whereas smaller particles (<146 nm) were not. Conclusions: Particle size appears to be a critical determinant of cell survival and iron-induced epithelial COX-2 expression. Iron compounds that present as both soluble and particulate forms may optimize bioavailability, but controlling aggregate size (<146 nm) could reduce inflammatory signaling. These findings may have important implications for cell culture systems and warrant in vivo validation in iron supplemental studies. Full article
(This article belongs to the Special Issue Iron Metabolism in Cells)
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18 pages, 6736 KB  
Article
Therapeutic Potential of Deferiprone–Resveratrol Hybrid (DFP-RVT) Against Hepatic Iron Overload in β-Thalassemia Mice: A Proteomic Analysis
by Supawadee Maneekesorn, Yodying Yingchutrakul, Nattapon Simanon, Jakkaphan Kumsab, Chutikarn Butkinaree, Sutpirat Moonmuang, Jin Li, Pimlak Charoenkwan, Pimpisid Koonyosying, Narisara Paradee, Somdet Srichairatanakool and Hataichanok Chuljerm
Biomolecules 2026, 16(2), 338; https://doi.org/10.3390/biom16020338 - 23 Feb 2026
Cited by 1 | Viewed by 1539
Abstract
Iron overload is a major pathological feature of β-thalassemia and a key driver of hepatic injury through oxidative stress and mitochondrial dysfunction. This study investigated the molecular effects of iron overload on liver mitochondria and evaluated the therapeutic potential of a deferiprone–resveratrol hybrid [...] Read more.
Iron overload is a major pathological feature of β-thalassemia and a key driver of hepatic injury through oxidative stress and mitochondrial dysfunction. This study investigated the molecular effects of iron overload on liver mitochondria and evaluated the therapeutic potential of a deferiprone–resveratrol hybrid (DFP-RVT) in a β-thalassemia mouse model. Proteomic analysis was performed on liver tissues from baseline control, iron-overloaded, and DFP-RVT-treated mice to identify differentially expressed proteins and affected pathways. Iron overload resulted in marked downregulation of mitochondrial proteins, particularly components of oxidative phosphorylation and iron–sulfur cluster-associated pathways, including frataxin. In contrast, DFP-RVT treatment restored the expression of multiple mitochondrial proteins involved in respiratory chain function and energy metabolism. Comparative proteomic profiling revealed opposing regulation patterns between iron-overloaded and DFP-RVT-treated groups, indicating recovery of mitochondrial integrity following iron chelation therapy. These findings suggest that iron-induced hepatic injury in β-thalassemia is closely linked to mitochondrial protein dysregulation and that DFP-RVT may mitigate this process by restoring mitochondrial protein expression and iron homeostasis. This study provides mechanistic insight into iron-mediated mitochondrial dysfunction and supports the therapeutic potential of DFP-RVT for iron overload-associated liver injury. Full article
(This article belongs to the Special Issue Iron Metabolism in Cells)
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Review

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16 pages, 1195 KB  
Review
Ferroportin at the Crossroads of Iron Biology: Disease, Regulation and Modulation
by Pramudi Hasanga Rathnayake, Nina E. Ryan, Ryan Atkins, Daniel F. Wallace and V. Nathan Subramaniam
Biomolecules 2026, 16(7), 1066; https://doi.org/10.3390/biom16071066 - 21 Jul 2026
Viewed by 668
Abstract
Iron is an essential element for almost all living beings. Ferroportin is the only known cellular iron exporter and is responsible for maintaining iron homeostasis. The hepcidin-ferroportin axis is central to iron regulation. Dysregulation of ferroportin is thus associated with iron disorders. Understanding [...] Read more.
Iron is an essential element for almost all living beings. Ferroportin is the only known cellular iron exporter and is responsible for maintaining iron homeostasis. The hepcidin-ferroportin axis is central to iron regulation. Dysregulation of ferroportin is thus associated with iron disorders. Understanding how ferroportin is regulated will provide greater insight into iron metabolism and potential therapies for iron-related disease. This review synthesizes current knowledge on ferroportin biology with a particular focus on its regulatory modulators and their therapeutic potential and provides an updated perspective on the molecular pathogenesis and clinical spectrum of ferroportin disease. Elucidating these mechanisms will be essential for the development of targeted interventions to correct iron dysregulation in diverse human diseases. Full article
(This article belongs to the Special Issue Iron Metabolism in Cells)
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22 pages, 2481 KB  
Review
Hepcidin as a Molecular Hub of Iron Homeostasis: From BMP–SMAD Signaling to Therapeutic Modulation
by Andrea Duminuco, Alessandro Costa, Federica Pilo, Salvatore Scarso, Cesarina Giallongo, Sebastiano Giallongo, Annalisa Santisi, Arianna Sbriglione, Laura Santocono, Giovanni Caocci and Giuseppe A. Palumbo
Biomolecules 2026, 16(7), 947; https://doi.org/10.3390/biom16070947 - 25 Jun 2026
Viewed by 1428
Abstract
Hepcidin, a 25-amino-acid peptide hormone produced primarily by hepatocytes, is the master regulator of systemic iron homeostasis. By binding the cellular iron exporter ferroportin and inducing its internalization and lysosomal degradation, hepcidin restricts iron entry into plasma from enterocytes, macrophages, and hepatocytes. Its [...] Read more.
Hepcidin, a 25-amino-acid peptide hormone produced primarily by hepatocytes, is the master regulator of systemic iron homeostasis. By binding the cellular iron exporter ferroportin and inducing its internalization and lysosomal degradation, hepcidin restricts iron entry into plasma from enterocytes, macrophages, and hepatocytes. Its transcription is governed by an intricate molecular network that integrates iron status, erythropoietic demand, oxygen tension, and inflammation, with the BMP–HJV–ALK2/SMAD axis acting as the canonical activating pathway and erythroferrone (ERFE) and matriptase-2 (TMPRSS6) as physiological suppressors. Dysregulation of hepcidin underpins a wide spectrum of human diseases: insufficient hepcidin drives hereditary hemochromatosis and the iron overload of congenital and acquired ineffective erythropoiesis diseases and other ineffective erythropoiesis syndromes, whereas excessive or inappropriate hepcidin contributes to anemia of inflammation, anemia of chronic kidney disease, iron-restricted erythropoiesis in cancer, the iron-restrictive anemia of myelofibrosis, and pathogen-restrictive nutritional immunity. Within the myeloproliferative neoplasm spectrum, the divergent hepcidin patterns observed in polycythemia vera (suppressed) and myelofibrosis (inappropriately elevated through dual BMP/ACVR1/SMAD and IL-6/STAT3 hyperactivation) exemplify the clinical relevance of this axis and underpin two opposite pharmacologic strategies. Over the past decade, hepcidin pathway pharmacology has matured from proof-of-concept to regulatory milestones, shifting perspectives on several diseases and markedly improving clinical approaches. Full article
(This article belongs to the Special Issue Iron Metabolism in Cells)
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