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Loss of alpha‐globin genes in human subjects is associated with improved nitric oxide‐mediated vascular perfusion

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Loss of alpha‐globin genes in human subjects is associated with improved nitric oxide‐mediated vascular perfusion

American Journal of Hematology

Fecha de publicación: 28 de noviembre de 2020

DOI: https://doi.org/10.1002/ajh.26058

Autores: Christopher C. Denton, Payal Shah, Silvie Suriany, Honglei Liu, Wanwara Thuptimdang, John Sunwoo, Patjanaporn Chalacheva, Saranya Veluswamy, Roberta Kato, John C. Wood, Jon A. Detterich, Michael C. K. Khoo, Thomas D. Coates

Background: Alpha thalassemia is a hemoglobinopathy due to decreased production of the α‐globin protein from loss of up to four α‐globin genes, with one or two missing in the trait phenotype. Individuals with sickle cell disease who co‐inherit the loss of one or two α‐globin genes have been known to have reduced risk of morbid outcomes, but the underlying mechanism is unknown. While α‐globin gene deletions affect sickle red cell deformability, the α‐globin genes and protein are also present in the endothelial wall of human arterioles and participate in nitric oxide scavenging during vasoconstriction.

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