Sickle Cell Disease: Pathogenesis and Therapies
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".
Deadline for manuscript submissions: 30 September 2026
Special Issue Editors
Interests: sickle cell disease; Hematology
2. Inserm U1163, Laboratory "Cellular and Molecular Mechanisms of Hematological Disorders and Therapeutic Implications", Imagine Institute, Paris Cité University, 75015 Paris, France
Interests: sickle cell disease; hematology
Special Issue Information
Dear Colleagues,
Since its emergence in prehistoric times in countries where malaria is endemic, sickle cell disease (SCD) has spread throughout the world, becoming the most common genetic disease globally.
SCD is caused by the homozygosity for the beta globin gene mutation (a substitution of valine for glutamic acid at position 6: β6 Glu→Val) or by compound heterozygosity in which one HbS allele is inherited together with another β-globin variant (e.g., HbSC, HbS/β⁰-thalassemia, HbS/β⁺-thalassemia,etc). Under physiological stress conditions such as hypoxia, infection, acidosis, or dehydration, HbS polymerizes within the red blood cells, resulting in erythrocytes deformation, a process known as sickling. Sickling promotes chronic hemolytic anemia and recurrent vaso-occlusion in small vessels, driving acute and chronic tissue injury, particularly in the bones and multiple organ systems.
Long overlooked and still not fully understood, SCD was first described in the United States in 1910, and it took over 80 years before the first disease-modifying therapy, hydroxyurea, was approved.
However, it would be simplistic to consider SCD merely as red blood cell disorder. Its pathophysiology also involves endothelial dysfunction, platelet activation, leukocyte adhesion, a procoagulant state, and chronic inflammation.
Current research aims to better define these interconnected pathways, which both shape clinical outcomes and represent promising targets for innovative therapies.
Allogeneic hematopoietic stem cell transplantation (HSCT) from HLA-matched sibling donors remains the only established curative option. However, its use is limited by donor availability. Recent advances in haploidentical transplantation and gene therapy are yielding encouraging results in clinical trials, although both approaches remain limited by the need of pre-transplantation conditioning and the restricted accessibility of these costly therapies.
Dr. Laure Joseph
Dr. Geoffrey Cheminet
Guest Editors
Manuscript Submission Information
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Keywords
- sickle cell disease
- erythrocyte sickling
- chronic inflammation
- endothelial dysfunction
- hematopoietic stem cell transplantation
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