ArticleBlood advances2019
Nox2 NADPH oxidase is dispensable for platelet activation or arterial thrombosis in mice.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 51 citations in OpenAlex.
- [Advances in research on the mechanisms of reactive oxygen species in platelet activation and thrombosis].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Redox Regulation of Megakaryocyte Differentiation and Platelet Biogenesis.Antioxidants (Basel, Switzerland) · 2026Review
- Redox Regulation of Microvascular Physiology and Pathophysiology: Insights into Therapeutic Strategies and Limitations.Antioxidants & redox signaling · 2025Review
- Mitochondrial Calcium Uniporter Regulates ITAM-Dependent Platelet Activation.Circulation research · 2025Article
- The Mitochondrial Permeability Transition Pore in Platelets: Mechanisms, Physiological Roles, and Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- The Fifth Annual Symposium of the Midwest Aging Consortium.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Nutritional Advantages of Walnut (Food science & nutrition · 2025Review
- Loss of endogenous Nox2-NADPH oxidase does not prevent age-induced platelet activation and arterial thrombosis in mice.Research and practice in thrombosis and haemostasis · 2024Article
- Aging-related alterations in mechanistic target of rapamycin signaling promote platelet hyperreactivity and thrombosis.Journal of thrombosis and haemostasis : JTH · 2024Article
- Extracellular histones: a unifying mechanism driving platelet-dependent extracellular vesicle release and thrombus formation in COVID-19.Journal of thrombosis and haemostasis : JTH · 2024Article
- Oxidative Stress Induced by Cortisol in Human Platelets.International journal of molecular sciences · 2024Article
- Inhibition of mitochondrial calcium transporters alters adp-induced platelet responses.Molecular biology reports · 2024Article
- Targeting Cysteine Oxidation in Thrombotic Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- NOX-2 Inhibitors may be Potential Drug Candidates for the Management of COVID-19 Complications.Current drug research reviews · 2024Review
- Sulfenylation links oxidative stress to protein disulfide isomerase oxidase activity and thrombus formation.Journal of thrombosis and haemostasis : JTH · 2023Article
- An Overview of Two Old Friends Associated with Platelet Redox Signaling, the Protein Disulfide Isomerase and NADPH Oxidase.Biomolecules · 2023Article
- Endogenous SOD2 (Superoxide Dismutase) Regulates Platelet-Dependent Thrombin Generation and Thrombosis During Aging.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Notch signaling functions in noncanonical juxtacrine manner in platelets to amplify thrombogenicity.eLife · 2022Article
- Platelet Redox Imbalance in Hypercholesterolemia: A Big Problem for a Small Cell.International journal of molecular sciences · 2022Review
- Noncanonical Sonic Hedgehog signaling amplifies platelet reactivity and thrombogenicity.Blood advances · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Deficiency of the Nox2 (gp91phox) catalytic subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a genetic cause of X-linked chronic granulomatous disease, a condition in which patients are prone to infection resulting from the loss of oxidant production by neutrophils. Some studies have suggested a role for superoxide derived from Nox2 NADPH oxidase in platelet activation and thrombosis, but data are conflicting. Using a rigorous and comprehensive approach, we tested the hypothesis that genetic deficiency of Nox2 attenuates platelet activation and arterial thrombosis. Our study was designed to test the genotype differences within male and female mice. Using chloromethyl-dichlorodihydrofluorescein diacetate, a fluorescent dye, as well as high-performance liquid chromatography analysis with dihydroethidium as a probe to detect intracellular reactive oxygen species (ROS), we observed no genotype differences in ROS levels in platelets. Similarly, there were no genotype-dependent differences in levels of mitochondrial ROS. In addition, we did not observe any genotype-associated differences in platelet activation, adhesion, secretion, or aggregation in male or female mice. Platelets from chronic granulomatous disease patients exhibited similar adhesion and aggregation responses as platelets from healthy subjects. Susceptibility to carotid artery thrombosis in a photochemical injury model was similar in wild-type and Nox2-deficient male or female mice. Our findings indicate that Nox2 NADPH oxidase is not an essential source of platelet ROS or a mediator of platelet activation or arterial thrombosis in large vessels, such as the carotid artery.
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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.