Regulation of Iron Homeostasis

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 20 May 2026 | Viewed by 1147

Special Issue Editor


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Guest Editor
Department of Biological Sciences, BMB Division, Louisiana State University, Baton Rouge, LA 70803, USA
Interests: iron-sulfur proteins; free iron; iron homeostasis

Special Issue Information

Dear Colleagues,

Iron is an indispensable trace element required by virtually all living organisms. It functions predominantly within proteins as part of mononuclear iron, iron–sulfur clusters, or heme prosthetic groups, facilitating a broad spectrum of physiological processes, including DNA replication and repair, RNA synthesis and modification, amino acid biosynthesis, co-factor biosynthesis, energy metabolism, and signal transduction. Despite its essential role, excessive accumulation of intracellular iron is deleterious, as ferrous iron can catalyze the formation of reactive oxygen species through the Fenton reaction under aerobic conditions, thereby inducing oxidative cellular damage. To mitigate these detrimental effects and provide accessible iron, organisms have evolved intricate regulatory networks that tightly control iron homeostasis through the coordinated regulation of iron uptake, transport, and storage. This Special Issue will highlight recent advances in elucidating the molecular mechanisms that underlie cellular iron homeostasis.

Prof. Dr. Huangen Ding
Guest Editor

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Keywords

  • iron homeostasis
  • iron transport
  • iron storage
  • iron-containing proteins

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Published Papers (1 paper)

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Review

20 pages, 1997 KB  
Review
Iron Deficiency in Immune-Mediated Inflammatory Skin Diseases: A Missing Link Between Systemic Inflammation, Immunometabolism, and Disease Burden
by Emilia Kucharczyk, Klara Andrzejczak, Karol Biliński, Matylda Korgiel and Małgorzata Ponikowska
Cells 2026, 15(5), 478; https://doi.org/10.3390/cells15050478 - 6 Mar 2026
Viewed by 884
Abstract
Iron deficiency (ID) has emerged as a pivotal yet underrecognized factor in the pathogenesis of immune-mediated inflammatory skin diseases (IMISDs) such as psoriasis, atopic dermatitis, and hidradenitis suppurativa. Beyond its classical role in erythropoiesis, iron acts as a key modulator of immune cell [...] Read more.
Iron deficiency (ID) has emerged as a pivotal yet underrecognized factor in the pathogenesis of immune-mediated inflammatory skin diseases (IMISDs) such as psoriasis, atopic dermatitis, and hidradenitis suppurativa. Beyond its classical role in erythropoiesis, iron acts as a key modulator of immune cell activity, redox balance, and overall metabolic homeostasis. This review synthesises the latest evidence on the intricate relationship between systemic inflammation, disturbances of iron metabolism, and immunometabolic imbalances that underline the pathogenesis of IMISDs. Findings indicate that chronic inflammation drives functional iron deficiency through IL-6–hepcidin-mediated sequestration of iron, resulting in reduced bioavailability and altered mitochondrial activity in immune and epithelial cells. This imbalance is associated with excessive and chronically enhanced oxidative and inflammatory responses of these cells, further advancing inflammation, anaemia of chronic disease, and disturbances of tissue repair. Moreover, emerging evidence supports an “iron-skin axis,” and suggests that skin cells, particularly epidermal keratinocytes, are actively involved in the regulation of iron pathways. Collectively, these insights position iron homeostasis as a missing link between systemic inflammation, immunometabolic imbalance, and disease burden in IMISDs. Full article
(This article belongs to the Special Issue Regulation of Iron Homeostasis)
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