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Biomedicines
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The Role of Iron in Human Diseases
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The Role of Iron in Human Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 1432

Special Issue Editor

Dr. Margherita Correnti

E-Mail Website
Guest Editor
Department of Biomedical Sciences for Health, University of Milan, 20133 Milan, Italy
Interests: iron; macrophages; tumor; liver; cholangiocarcinoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Iron is an essential element for several biological processes. Iron balance is strictly regulated because both the excess and deficiency of iron are toxic. Abnormalities in systemic and/or cellular iron balance are common in many diseases. This Special Issue will offer an overview of the essential role of iron in biology. Moreover, it will provide insights into the changes occurring in iron metabolism during different pathological conditions, as well as into how imbalances in iron homeostasis contribute to diseases. Finally, the Special Issue will also aim to explore how a dysregulation in iron metabolism may influence other metabolic pathways.

Dr. Margherita Correnti
Guest Editor

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Keywords

  • iron metabolism
  • iron dysregulation
  • diseases
  • iron deficiency
  • iron overload

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Published Papers (3 papers)

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Research

20 pages, 5004 KiB  
Article
Maresin1 Alleviates Ischemia Reperfusion Injury After Lung Transplantation by Inhibiting Ferroptosis via the PKA-Hippo-YAP Signaling Pathway
by Peng Deng, You Wu, Li Wan, Xiangfu Sun and Quanchao Sun
Biomedicines 2025, 13(7), 1594; https://doi.org/10.3390/biomedicines13071594 - 30 Jun 2025
Viewed by 260
Abstract
Background: Lung ischemia reperfusion injury (LIRI) is a severe complication after lung transplantation (LT). Ferroptosis contributes to the pathogenesis of LIRI. Maresin1 (MaR1) is an endogenous pro-resolving lipid mediator that exerts protective effects against multiorgan diseases. However, the role and mechanism of [...] Read more.
Background: Lung ischemia reperfusion injury (LIRI) is a severe complication after lung transplantation (LT). Ferroptosis contributes to the pathogenesis of LIRI. Maresin1 (MaR1) is an endogenous pro-resolving lipid mediator that exerts protective effects against multiorgan diseases. However, the role and mechanism of MaR1 in the ferroptosis of LIRI after LT need to be further investigated. Methods: A mouse LT model and a pulmonary vascular endothelial cell line after hypoxia reoxygenation (H/R) culture were established in our study. Histological morphology and inflammatory cytokine levels predicted the severity of LIRI. Cell viability and cell injury were determined by CCK-8 and LDH assays. Ferroptosis biomarkers, including Fe2+, MDA, 4-HNE, and GSH, were assessed by relevant assay kits. Transferrin receptor (TFRC) and Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) protein levels were examined by western blotting. In vitro, lipid peroxide levels were detected by DCFH-DA staining and flow cytometry analysis. The ultrastructure of mitochondria was imaged using transmission electron microscopy. Furthermore, the potential mechanism by which MaR1 regulates ferroptosis was explored and verified with signaling pathway inhibitors using Western blotting. Results: MaR1 protected mice from LIRI after LTx, which was reversed by the ferroptosis agonist Sorafenib in vivo. MaR1 administration decreased Fe2+, MDA, 4-HNE, TFRC, and ACSL4 contents, increased GSH levels, and ameliorated mitochondrial ultrastructural injury after LTx. In vitro, Sorafenib resulted in lower cell viability and worsened cell injury and enhanced the hallmarks of ferroptosis after H/R culture, which was rescued by MaR1 treatment. Mechanistically, the protein kinase A and YAP inhibitors partly blocked the effects of MaR1 on ferroptosis inhibition and LIRI protection. Conclusions: This study revealed that MaR1 alleviates LIRI and represses ischemia reperfusion-induced ferroptosis via the PKA-Hippo-YAP signaling pathway, which may offer a promising theoretical basis for the clinical application of organ protection after LTx. Full article
(This article belongs to the Special Issue The Role of Iron in Human Diseases)
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14 pages, 3817 KiB  
Article
Mechanism of Circadian Regulation in Ferroptosis of the BMAL1/NRF2 Pathway in Renal Ischemia–Reperfusion
by Shang Xu, Qiao Tang, Haiyang Du, Jiatao Xie, Ruoxin He, Ruiyan Wang and Qian Sun
Biomedicines 2025, 13(6), 1375; https://doi.org/10.3390/biomedicines13061375 - 4 Jun 2025
Viewed by 527
Abstract
Background: Renal ischemia–reperfusion injury (IRI) is a frequent cause of kidney transplant failure. Recent studies have shown that the extent of injury is closely linked to ferroptosis, and the process of cellular ferroptosis is diurnal and regulated by circadian genes. NRF2, [...] Read more.
Background: Renal ischemia–reperfusion injury (IRI) is a frequent cause of kidney transplant failure. Recent studies have shown that the extent of injury is closely linked to ferroptosis, and the process of cellular ferroptosis is diurnal and regulated by circadian genes. NRF2, involved in iron–heme metabolism, may be related to ferroptosis. We hypothesize that the pathway plays a role in circadian regulation in ferroptosis in renal IRI. Methods: Using hematoxylin and eosin (H&E) staining, enzyme-linked immunosorbent assay (ELISA), Cell Counting Kit-8 (CCK8), flow cytometry, real-time quantitative reverse transcription PCR (qRT-PCR), and Western blotting, we analyzed renal tubular tissues in vivo and in vitro and compared the groups with IR injury treatment, inhibition of ferroptosis, and inhibition of BMAL1 gene expression at the ZT0 (zeitgeber time 0) and ZT12 (zeitgeber time 12) time points. Results: IR injury treatments caused exacerbation of injury, both in vivo and in vitro, and were more pronounced at the ZT12 time point, which correlates with circadian rhythms. The use of the ferroptosis inhibitor (Fer-I) attenuated IR injury, suggesting that IRI is associated with ferroptosis. In contrast, reduced BMAL1-gene expression exacerbated injury, and NRF2, which is elevated in IR injury, was suppressed. Conclusions: The circadian gene BMAL1 affects the circadian rhythm of ferroptosis in renal IRI through the regulation of NRF2 and its downstream pathway. In this study, renal injury is well ameliorated by the ferroptosis inhibitor, exhibiting potential as a therapeutic agent for use in renal transplantation. Full article
(This article belongs to the Special Issue The Role of Iron in Human Diseases)
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16 pages, 3615 KiB  
Article
Targeting RPLP2 Triggers DLBCL Ferroptosis by Decreasing FXN Expression
by Jiaxing Guo, Bokang Yan, Lingshu Li, Yuanhao Peng, Weiwei Lai and Chanjuan Shen
Biomedicines 2025, 13(6), 1320; https://doi.org/10.3390/biomedicines13061320 - 28 May 2025
Viewed by 376
Abstract
Background/Objectives: Ribosomal Protein Lateral Stalk Subunit P2 (RPLP2), an important ribosomal protein, is mainly involved in modulating protein synthesis and plays an essential role in the carcinogenesis of many cancers. However, its precise impact on diffuse large B-cell lymphoma (DLBCL) remains unknown. Methods: [...] Read more.
Background/Objectives: Ribosomal Protein Lateral Stalk Subunit P2 (RPLP2), an important ribosomal protein, is mainly involved in modulating protein synthesis and plays an essential role in the carcinogenesis of many cancers. However, its precise impact on diffuse large B-cell lymphoma (DLBCL) remains unknown. Methods: This study utilized siRNA to knock down RPLP2, aiming to investigate its role in DLBCL progression. RT-qPCR and immunohistochemistry (IHC) were employed to assess RPLP2 and frataxin (FXN) expression levels in DLBCL. CCK8 and colony formation assays measured cell proliferation inhibition upon RPLP2 deletion, while transwell migration assays analyzed reduced cell motility. Lipid ROS and iron assays quantified ferroptosis markers to elucidate RPLP2’s regulation of FXN-mediated ferroptosis. Xenograft mouse models validated tumor suppression effects in vivo. Results: Here, we reveal that elevated RPLP2 expression is significantly correlated to unfavorable prognosis in DLBCL patients. In addition, we demonstrate that RPLP2 deletion dramatically reduces the cell proliferation and migration of DLBCL. Besides, knockdown of RPLP2 triggers ferroptosis via regulating ferroptosis suppressor FXN activity. Moreover, we discover that Destruxin b could target RPLP2 to suppress the development of DLBCL. Lastly, the combination of Destruxin b with Dox remarkably improves the anti-tumor effect. Conclusions: In general, the present study reveals the oncogenic role of RPLP2 in DLBCL, uncovers an unrecognized regulatory axis of ferroptosis, and identifies a specific inhibitor targeting RPLP2 to restrain DLBCL progression, suggesting that RPLP2 could be a potential target for DLBCL treatment. Full article
(This article belongs to the Special Issue The Role of Iron in Human Diseases)
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