Highlights in Red Blood Cell Research

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

Deadline for manuscript submissions: 30 June 2025 | Viewed by 12623

Special Issue Editors


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Guest Editor
Red Blood Cell Research Group, Institute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Zürich, Switzerland
Interests: red blood cells; hypoxia; heterogeneity; redox signaling; anemia
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Special Issue Information

Dear Colleagues,

This Special Issue welcomes articles exploring novel aspects of red blood cell research that address the following topics: (i) fundamental aspects of red blood cell structure and function; (ii) pathology associated with red blood cell disorders; (iii) red cell conservation, de novo production, and transfusion; and (iv) adaptation of red blood cells in humans and animals to environmental changes. We also welcome papers on novel technologies for studying red blood cells.

Prof. Dr. Anna Bogdanova
Prof. Dr. Lars Kaestner
Guest Editors

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Keywords

  • red blood cells
  • anemia
  • transfusion
  • erythropoiesis
  • signaling

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Published Papers (3 papers)

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Research

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22 pages, 5018 KiB  
Article
Hematin- and Hemin-Induced Spherization and Hemolysis of Human Erythrocytes Are Independent of Extracellular Calcium Concentration
by Diana M. Mikhailova, Elisaveta Skverchinskaya, Julia Sudnitsyna, Kirill R. Butov, Ekaterina M. Koltsova, Igor V. Mindukshev and Stepan Gambaryan
Cells 2024, 13(6), 554; https://doi.org/10.3390/cells13060554 - 21 Mar 2024
Cited by 2 | Viewed by 2582
Abstract
Pathologies such as malaria, hemorrhagic stroke, sickle cell disease, and thalassemia are characterized by the release of hemoglobin degradation products from damaged RBCs. Hematin (liganded with OH) and hemin (liganded with Cl)—are the oxidized forms of heme with toxic [...] Read more.
Pathologies such as malaria, hemorrhagic stroke, sickle cell disease, and thalassemia are characterized by the release of hemoglobin degradation products from damaged RBCs. Hematin (liganded with OH) and hemin (liganded with Cl)—are the oxidized forms of heme with toxic properties due to their hydrophobicity and the presence of redox-active Fe3. In the present study, using the original LaSca-TM laser particle analyzer, flow cytometry, and confocal microscopy, we showed that both hematin and hemin induce dose-dependent RBC spherization and hemolysis with ghost formation. Hematin and hemin at nanomolar concentrations increased [Ca2+]i in RBC; however, spherization and hemolysis occurred in the presence and absence of calcium, indicating that both processes are independent of [Ca2+]i. Both compounds triggered acute phosphatidylserine exposure on the membrane surface, reversible after 60 min of incubation. A comparison of hematin and hemin effects on RBCs revealed that hematin is a more reactive toxic metabolite than hemin towards human RBCs. The toxic effects of heme derivatives were reduced and even reversed in the presence of albumin, indicating the presence in RBCs of the own recovery system against the toxic effects of heme derivatives. Full article
(This article belongs to the Special Issue Highlights in Red Blood Cell Research)
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Review

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14 pages, 1052 KiB  
Review
The Role of Erythropoietin in Metabolic Regulation
by Weiqin Yin and Constance T. Noguchi
Cells 2025, 14(4), 280; https://doi.org/10.3390/cells14040280 - 14 Feb 2025
Viewed by 1251
Abstract
Erythropoietin (EPO) is a key regulator of erythrocyte production, promoting erythroid progenitor cell survival, division, and differentiation in the fetal liver and adult bone marrow. Mice lacking EPO or its receptor (EPOR) die in utero due to severe anemia. Beyond hematopoiesis, EPO influences [...] Read more.
Erythropoietin (EPO) is a key regulator of erythrocyte production, promoting erythroid progenitor cell survival, division, and differentiation in the fetal liver and adult bone marrow. Mice lacking EPO or its receptor (EPOR) die in utero due to severe anemia. Beyond hematopoiesis, EPO influences non-hematopoietic tissues, including glucose and fat metabolism in adipose tissue, skeletal muscle, and the liver. EPO is used to treat anemia associated with chronic kidney disease clinically and plays a role in maintaining metabolic homeostasis and regulating fat mass. EPO enhances lipolysis while inhibiting lipogenic gene expression in white adipose tissue, brown adipose tissue, skeletal muscle, and the liver, acting through the EPO-EPOR-RUNX1 axis. The non-erythroid EPOR agonist ARA290 also improves diet-induced obesity and glucose tolerance providing evidence for EPO regulation of fat metabolism independent of EPO stimulated erythropoiesis. Therefore, in addition to the primary role of EPO to stimulate erythropoiesis, EPO contributes significantly to EPOR-dependent whole-body metabolic response. Full article
(This article belongs to the Special Issue Highlights in Red Blood Cell Research)
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19 pages, 1519 KiB  
Review
Current and Future Therapeutics for Treating Patients with Sickle Cell Disease
by Mariam Barak, Christopher Hu, Alicia Matthews and Yolanda M. Fortenberry
Cells 2024, 13(10), 848; https://doi.org/10.3390/cells13100848 - 16 May 2024
Cited by 9 | Viewed by 7967
Abstract
Sickle cell disease (SCD) is the most common genetic blood disorder in the United States, with over 100,000 people suffering from this debilitating disease. SCD is caused by abnormal hemoglobin (Hb) variants that interfere with normal red blood cell (RBC) function. Research on [...] Read more.
Sickle cell disease (SCD) is the most common genetic blood disorder in the United States, with over 100,000 people suffering from this debilitating disease. SCD is caused by abnormal hemoglobin (Hb) variants that interfere with normal red blood cell (RBC) function. Research on SCD has led to the development and approval of several new SCD therapies in recent years. The recent FDA-approved novel gene therapies are potentially curative, giving patients an additional option besides a hematopoietic bone marrow transplant. Despite the promise of existing therapies, questions remain regarding their long-term pharmacological effects on adults and children. These questions, along with the exorbitant cost of the new gene therapies, justify additional research into more effective therapeutic options. Continual research in this field focuses on not only developing cheaper, more effective cures/treatments but also investigating the physiological effects of the current therapies on SCD patients, particularly on the brain and kidneys. In this article, we undertake a comprehensive review of ongoing clinical trials with completion dates in 2024 or later. Our exploration provides insights into the landscape of current therapeutics and emerging novel therapies designed to combat and potentially eradicate SCD, including the latest FDA-approved gene therapies. Full article
(This article belongs to the Special Issue Highlights in Red Blood Cell Research)
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