ArticleClinical hemorheology and microcirculation2018
Nitric oxide pathology and therapeutics in sickle cell disease.
Article in Clinical hemorheology and microcirculation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Zinc level and its impact on the phenotype of sickle cell disease.Annals of hematology · 2025Trial
- Alterations of Plasma Metabolites Associated with Sickle Cell Trait.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- Review
- Article
- Systematic Review of Extracorporeal Membrane Oxygenation in Adult Sickle Cell Disease.Journal of clinical medicine · 2025Review
- Sex and genotype specificities of microvasculature and muscle remodeling in sub-Saharan sickle cell trait and disease.Blood advances · 2025Article
- Redox Homeostasis in Red Blood Cells: From Molecular Mechanisms to Antioxidant Strategies.Current issues in molecular biology · 2025Review
- Review
- Effects ofLife (Basel, Switzerland) · 2024Article
- The clinical spectrum of HbSC sickle cell disease-not a benign condition.British journal of haematology · 2024Article
- Article
- Design, Synthesis, and Antisickling Investigation of a Nitric Oxide-Releasing Prodrug of 5HMF for the Treatment of Sickle Cell Disease.Biomolecules · 2022Article
- Testosterone Deficiency in Sickle Cell Disease: Recognition and Remediation.Frontiers in endocrinology · 2022Review
- Red Blood Cell and Endothelial eNOS Independently Regulate Circulating Nitric Oxide Metabolites and Blood Pressure.Circulation · 2021Article
- Alpha thalassemia, but not βAnnals of hematology · 2021Article
- One-Fifth of Children with Sickle Cell Anemia Show Exercise-Induced Hemoglobin Desaturation: Rate of Perceived Exertion and Role of Blood Rheology.Journal of clinical medicine · 2020Article
- Sickle cell disease subjects and mouse models have elevated nitrite and cGMP levels in blood compartments.Nitric oxide : biology and chemistry · 2020Article
- Impact of A Six Week Training Program on Ventilatory Efficiency, Red Blood Cell Rheological Parameters and Red Blood Cell Nitric Oxide Signaling in Young Sickle Cell Anemia Patients: A Pilot Study.Journal of clinical medicine · 2019Article
- cGMP modulation therapeutics for sickle cell disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- New Therapeutic Options for the Treatment of Sickle Cell Disease.Mediterranean journal of hematology and infectious diseases · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Sickle cell disease is caused by a mutant form of hemoglobin that polymerizes under hypoxic conditions which leads to red blood cell (RBC) distortion, calcium-influx mediated RBC dehydration, increased RBC adhesivity, reduced RBC deformability, increased RBC fragility, and hemolysis. These impairments in RBC structure and function result in multifaceted downstream pathology including inflammation, endothelial cell activation, platelet and leukocyte activation and adhesion, and thrombosis, all of which contribute vascular occlusion and substantial morbidity and mortality. Hemoglobin released upon RBC hemolysis scavenges nitric oxide (NO) and generates reactive oxygen species (ROS) and thereby decreases bioavailability of this important signaling molecule. As the endothelium-derived relaxing factor, NO acts as a vasodilator and also decreases platelet, leukocyte, and endothelial cell activation. Thus, low NO bioavailability contributes to pathology in sickle cell disease and its restoration could serve as an effective treatment. Despite its promise, clinical trials based on restoring NO bioavailability have so far been mainly disappointing. However, particular "NO donating" agents such as nitrite, which unlike some other NO donors can improve sickle RBC properties, may yet prove effective.
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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.