ArticleArteriosclerosis, thrombosis, and vascular biology2014
NADPH oxidase-generated reactive oxygen species are required for stromal cell-derived factor-1α-stimulated angiogenesis.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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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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.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
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- Structure, regulation, and physiological functions of NADPH oxidase 5 (NOX5).Journal of physiology and biochemistry · 2023Review
- Review
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- NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology.Antioxidants (Basel, Switzerland) · 2021Review
- Oxidative Stress and Hypertension.Circulation research · 2021Review
- NOX5-induced uncoupling of endothelial NO synthase is a causal mechanism and theragnostic target of an age-related hypertension endotype.PLoS biology · 2020Article
- Interrelation between ROS and CaRedox biology · 2020Review
- NOX5: Molecular biology and pathophysiology.Experimental physiology · 2019Review
- NADPH Oxidase 5 Is a Pro-Contractile Nox Isoform and a Point of Cross-Talk for Calcium and Redox Signaling-Implications in Vascular Function.Journal of the American Heart Association · 2018Article
- Proanthocyanidins against Oxidative Stress: From Molecular Mechanisms to Clinical Applications.BioMed research international · 2018Review
- Palmitic acid dysregulates the Hippo-YAP pathway and inhibits angiogenesis by inducing mitochondrial damage and activating the cytosolic DNA sensor cGAS-STING-IRF3 signaling mechanism.The Journal of biological chemistry · 2017Article
- NADPH Oxidases, Angiogenesis, and Peripheral Artery Disease.Antioxidants (Basel, Switzerland) · 2017Review
- Roles of Nicotinamide Adenine Dinucleotide Phosphate (NADPH) Oxidase in Angiogenesis: Isoform-Specific Effects.Antioxidants (Basel, Switzerland) · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveReactive oxygen species (ROS) act as signaling molecules during angiogenesis; however, the mechanisms used for such signaling events remain unclear. Stromal cell-derived factor-1α (SDF-1α) is one of the most potent angiogenic chemokines. Here, we examined the role of ROS in the regulation of SDF-1α-dependent angiogenesis. APPROACH AND
resultsBovine aortic endothelial cells were treated with SDF-1α, and intracellular ROS generation was monitored. SDF-1α treatment induced bovine aortic endothelial cell migration and ROS generation, with the majority of ROS generated by bovine aortic endothelial cells at the leading edge of the migratory cells. Antioxidants and nicotinamide adenine dinucleotide phosphate oxidase (NOX) inhibitors blocked SDF-1α-induced endothelial migration. Furthermore, knockdown of either NOX5 or p22phox (a requisite subunit for NOX1/2/4 activation) significantly impaired endothelial motility and tube formation, suggesting that multiple NOXs regulate SDF-1α-dependent angiogenesis. Our previous study demonstrated that c-Jun N-terminal kinase 3 activity is essential for SDF-1α-dependent angiogenesis. Here, we identified that NOX5 is the dominant NOX required for SDF-1α-induced c-Jun N-terminal kinase 3 activation and that NOX5 and MAP kinase phosphatase 7 (MKP7; the c-Jun N-terminal kinase 3 phosphatase) associate with one another but decrease this interaction on SDF-1α treatment. Furthermore, MKP7 activity was inhibited by SDF-1α, and this inhibition was relieved by NOX5 knockdown, indicating that NOX5 promotes c-Jun N-terminal kinase 3 activation by blocking MKP7 activity.
conclusionsWe conclude that NOX is required for SDF-1α signaling and that intracellular redox balance is critical for SDF-1α-induced endothelial migration and angiogenesis.
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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.