ArticleExperimental biology and medicine (Maywood, N.J.)2016
Original Research: Diametric effects of hypoxia on pathophysiology of sickle cell disease in a murine model.
Article in Experimental biology and medicine (Maywood, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Smooth muscle cytochrome b5 reductase 3 deficiency accelerates pulmonary hypertension development in sickle cell mice.Blood advances · 2019Article
- Sickle cell disease severity: an introduction.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Experimental intravascular hemolysis induces hemodynamic and pathological pulmonary hypertension: association with accelerated purine metabolism.Pulmonary circulationArticle
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Hypoxia causes erythrocyte sickling in vitro; however, its role in the pathophysiology of sickle cell disease is poorly understood. We report that hypoxia rapidly decreased oxygen saturation in transgenic sickle cell disease mice, but this effect was immediately buffered by a robust ventilatory response. The initial hypoxemia improved steadily throughout the duration of hypoxia without any detectable acute pulmonary adverse effect. Furthermore, the mice suffered acute anemia that ironically was associated with lowering of both plasma hemoglobin and heme. These results were corroborated by increased plasma haptoglobin and hemopexin levels. Markers of ischemic tissue injury increased spatiotemporally following repeated hypoxia exposures. This variation was supported by organ-specific induction of hypoxia-responsive genes. Our results show that hypoxia exerts diametric effects on sickle cell disease by promoting ischemic injury while enhancing the expression of hemolysis scavenger molecules. This phenomenon may help to understand the disparate clinical syndromes associated with hemolysis and vaso-occlusion in sickle cell disease.
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