ReviewAmerican journal of hematology2021
Multiple inducers of endothelial NOS (eNOS) dysfunction in sickle cell disease.
Review in American journal of hematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Breaking the vicious cycle in sickle cell disease: Redox stress impairs red blood cell rheology and promotes lung vasocongestion.Free radical biology & medicine · 2025Article
- Clotting, inflammation, and immunity: the multifaceted role of platelets in HIV and sickle cell disease - a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Management of liver sinusoidal obstruction syndrome/veno-occlusive disease in adults: a 2025 perspective from an international expert group.Bone marrow transplantation · 2025Review
- The Link Between Venous and Arterial Thrombosis: Is There a Role for Endothelial Dysfunction?Cells · 2025Review
- Pharmacogenomics of Drugs Used in β-Thalassemia and Sickle-Cell Disease: From Basic Research to Clinical Applications.International journal of molecular sciences · 2024Review
- Sterile inflammation induces vasculopathy and chronic lung injury in murine sickle cell disease.Free radical biology & medicine · 2024Article
- Dysregulated complement activation during acute myocardial infarction leads to endothelial glycocalyx degradation and endothelial dysfunction via the C5a:C5a-Receptor1 axis.Frontiers in immunology · 2024Article
- Multi-Organ Morphological Findings in a Humanized Murine Model of Sickle Cell Trait.International journal of molecular sciences · 2023Article
- Assessment of Reticulocyte and Erythrocyte Parameters From Automated Blood Counts in Vaso-Occlusive Crisis on Sickle Cell Disease.Frontiers in medicine · 2022Article
- Multiple inducers of endothelial NOS (eNOS) dysfunction in sickle cell disease.American journal of hematology · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A characteristic aspect of the robust, systemic inflammatory state in sickle cell disease is dysfunction of endothelial nitric oxide synthase (eNOS). We identify 10 aberrant endothelial cell inputs, present in the specific sickle context, that are known to have the ability to cause eNOS dysfunction. These are: endothelial arginase depletion, asymmetric dimethylarginine, complement activation, endothelial glycocalyx degradation, free fatty acids, inflammatory mediators, microparticles, oxidized low density lipoproteins, reactive oxygen species, and Toll-like receptor 4 signaling ligands. The effect of true eNOS dysfunction on clinical testing using flow-mediated dilation can be simulated by two known examples of endothelial dysfunction mimicry (hemoglobin consumption of NO; and oxidation of smooth muscle cell soluble guanylate cyclase). This lends ambiguity to interpretation of such clinical testing. The presence of these multiple perturbing factors argues that a therapeutic approach targeting only a single injurious endothelial input (or either example of mimicry) would not be sufficiently efficacious. This would seem to argue for identifying therapeutics that directly protect eNOS function or application of multiple therapeutic approaches.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.