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- Melissa Azul, Eudorah F Vital, Wilbur A Lam, David K Wood, and Joan D Beckman.
- Department of Pediatrics, Mayo Clinic, Rochester, Minnesota.
- Transl Res. 2022 Aug 1; 246: 1141-14.
AbstractSickle cell disease (SCD) is caused by a single point mutation in the β-globin gene of hemoglobin, which produces an altered sickle hemoglobin (HbS). The ability of HbS to polymerize under deoxygenated conditions gives rise to chronic hemolysis, oxidative stress, inflammation, and vaso-occlusion. Herein, we review recent findings using microfluidic technologies that have elucidated mechanisms of oxygen-dependent and -independent induction of HbS polymerization and how these mechanisms elicit the biophysical and inflammatory consequences in SCD pathophysiology. We also discuss how validation and use of microfluidics in SCD provides the opportunity to advance development of numerous therapeutic strategies, including curative gene therapies.Copyright © 2022 Elsevier Inc. All rights reserved.
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