ArticleAtherosclerosis2015
Selective inactivation of NADPH oxidase 2 causes regression of vascularization and the size and stability of atherosclerotic plaques.
Article in Atherosclerosis, 2015. 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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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
35 citing papers in PubMed, 55 citations in OpenAlex.
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- The Dual Role of Oxidative Stress in Atherosclerosis and Coronary Artery Disease: Pathological Mechanisms and Diagnostic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Effects of colchicine adjuvant therapy on disease control, serum NALP3, sICAM-1, MMP-9 and MMP-13 in patients with coronary heart disease and acute gout attack.Journal of medical biochemistry · 2025Article
- Abnormal lipid metabolism and atherosclerosis: a new perspective on organelle function regulation and ferroptosis.Frontiers in immunology · 2025Article
- ICI-induced cardiovascular toxicity: mechanisms and immune reprogramming therapeutic strategies.Frontiers in immunology · 2025Review
- NADPH Oxidase 5 (NOX5) Upregulates MMP-10 Production and Cell Migration in Human Endothelial Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Recent progress of endoplasmic reticulum stress in the mechanism of atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
- Studies on the Effects of Hypercholesterolemia on Mouse Ophthalmic Artery Reactivity.Diseases (Basel, Switzerland) · 2023Article
- NADPH Oxidases: From Molecular Mechanisms to Current Inhibitors.Journal of medicinal chemistry · 2023Review
- Neutrophil-specific STAT4 deficiency attenuates atherosclerotic burden and improves plaque stability via reduction in neutrophil activation and recruitment into aortas ofbioRxiv : the preprint server for biology · 2023Article
- Neutrophil-specific STAT4 deficiency attenuates atherosclerotic burden and improves plaque stability via reduction in neutrophil activation and recruitment into aortas ofFrontiers in cardiovascular medicine · 2023Article
- Role of Oxidative Stress in the Pathogenesis of Atherothrombotic Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Role of oxidative stress in calcific aortic valve disease and its therapeutic implications.Cardiovascular research · 2022Review
- Identification of potential drug targets for vascular dementia and carotid plaques by analyzing underlying molecular signatures shared by them.Frontiers in aging neuroscience · 2022Article
- Calcium Dobesilate Modulates PKCδ-NADPH Oxidase- MAPK-NF-κB Signaling Pathway to ReduceAntioxidants (Basel, Switzerland) · 2021Article
- Potential Protective Effects of Equol (Soy Isoflavone Metabolite) on Coronary Heart Diseases-From Molecular Mechanisms to Studies in Humans.Nutrients · 2021Review
- NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology.Antioxidants (Basel, Switzerland) · 2021Review
- Different Approaches in Therapy Aiming to Stabilize an Unstable Atherosclerotic Plaque.International journal of molecular sciences · 2021Review
- Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure.International journal of molecular sciences · 2021Review
- Statins Mitigate Stress-Related Vascular Aging and Atherosclerosis inFrontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundA variety of NADPH oxidase (Nox) isoforms including Noxs 1, 2, 4 and 5 catalyze the formation of reactive oxygen species (ROS) in the vascular wall. The Nox2 isoform complex has arguably received the greatest attention in the progression of atherogenesis in animal models. Thus, in the current study we postulated that specific Nox2 oxidase inhibition could reverse or attenuate atherosclerosis in mice fed a high-fat diet.
methodsWe evaluated the effect of isoform-selective Nox2 assembly inhibitor on the progression and vascularization of atheromatous plaques. Apolipoprotein E-deficient mice (ApoE-/-) were fed a high fat diet for two months and treated over 15 days with Nox2ds-tat or control sequence (scrambled); 10 mg/kg/day, i.p. Mice were sacrificed and superoxide production in arterial tissue was detected by cytochrome C reduction assay and dihydroethidium staining. Plaque development was evaluated and the angiogenic markers VEGF, HIF1-α and visfatin were quantified by real time qRT-PCR. MMP-9 protein release and gelatinolytic activity was determined as a marker for vascularization.
resultsNox2ds-tat inhibited Nox-derived superoxide determined by cytochrome C in carotid arteries (2.3 ± 0.1 vs 1.7 ± 0.1 O2(•-) nmol/min*mg protein; P < 0.01) and caused a significant regression in atherosclerotic plaques in aorta (66 ± 6 μm(2) vs 37 ± 1 μm(2); scrmb vs. Nox2ds-tat; P < 0.001). Increased VEGF, HIF-1α, MMP-9 and visfatin expression in arterial tissue in response to high-fat diet were significantly attenuated by Nox2ds-tat which in turn impaired both MMP-9 protein expression and activity.
conclusionGiven these results, it is quite evident that selective Nox inhibitors can reverse vascular pathology arising with atherosclerosis.
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