ArticleRedox biology2018
The NADPH organizers NoxO1 and p47phox are both mediators of diabetes-induced vascular dysfunction in mice.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- The role of neurovascular coupling dysfunction in cognitive decline of diabetes patients.Frontiers in neuroscience · 2024Review
- Chronic SIRT1 supplementation in diabetic mice improves endothelial function by suppressing oxidative stress.Cardiovascular research · 2023Article
- GDF11 promotes wound healing in diabetic mice via stimulating HIF-1ɑ-VEGF/SDF-1ɑ-mediated endothelial progenitor cell mobilization and neovascularization.Acta pharmacologica Sinica · 2023Article
- Reactivity of renal and mesenteric resistance vessels to angiotensin II is mediated by NOXA1/NOX1 and superoxide signaling.American journal of physiology. Renal physiology · 2023Article
- A predicted structure of NADPH Oxidase 1 identifies key components of ROS generation and strategies for inhibition.PloS one · 2023Article
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Oxidative Injury in Ischemic Stroke: A Focus on NADPH Oxidase 4.Oxidative medicine and cellular longevity · 2022Review
- Astragaloside IV prevents endothelial dysfunction by improving oxidative stress in streptozotocin-induced diabetic mouse aortas.Experimental and therapeutic medicine · 2021Article
- Article
- Protective Effects of Hu-Lu-Ba-Wan () against Oxidative Stress in Testis of Diabetic Rats through PKCα/NAPDH Oxidase Signaling Pathway.Chinese journal of integrative medicine · 2021Article
- Oxidative Stress and Vascular Damage in the Context of Obesity: The Hidden Guest.Antioxidants (Basel, Switzerland) · 2021Review
- NCF1/2/4 Are Prognostic Biomarkers Related to the Immune Infiltration of Kidney Renal Clear Cell Carcinoma.BioMed research international · 2021Article
- Deletion of NoxO1 limits atherosclerosis development in female mice.Redox biology · 2020Article
- NADPH oxidases: Current aspects and tools.Redox biology · 2020Review
- Regulation of Vascular Function and Inflammation via Cross Talk of Reactive Oxygen and Nitrogen Species from Mitochondria or NADPH Oxidase-Implications for Diabetes Progression.International journal of molecular sciences · 2020Review
- NoxO1 Knockout Promotes Longevity in Mice.Antioxidants (Basel, Switzerland) · 2020Article
- Oxymatrine Ameliorates Memory Impairment in Diabetic Rats by Regulating Oxidative Stress and Apoptosis: Involvement of NOX2/NOX4.Oxidative medicine and cellular longevity · 2020Article
- Inhibition of miR-383 suppresses oxidative stress and improves endothelial function by increasing sirtuin 1.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Differential contribution of Nox1, Nox2 and Nox4 to kidney vascular oxidative stress and endothelial dysfunction in obesity.Redox biology · 2020Article
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimNADPH oxidases are important sources of reactive oxygen species (ROS). Several Nox homologues are present together in the vascular system but whether they exhibit crosstalk at the activity level is unknown. To address this, vessel function of knockout mice for the cytosolic Nox organizer proteins p47phox, NoxO1 and a p47phox-NoxO1-double knockout were studied under normal condition and during streptozotocin-induced diabetes.
resultsIn the mouse aorta, mRNA expression for NoxO1 was predominant in smooth muscle and endothelial cells, whereas p47phox was markedly expressed in adventitial cells comprising leukocytes and tissue resident macrophages. Knockout of either NoxO1 or p47phox resulted in lower basal blood pressure. Deletion of any of the two subunits also prevented diabetes-induced vascular dysfunction. mRNA expression analysis by MACE (Massive Analysis of cDNA ends) identified substantial gene expression differences between the mouse lines and in response to diabetes. Deletion of p47phox induced inflammatory activation with increased markers of myeloid cells and cytokine and chemokine induction. In contrast, deletion of NoxO1 resulted in an attenuated interferon gamma signature and reduced expression of genes related to antigen presentation. This aspect was also reflected by a reduced number of circulating lymphocytes in NoxO1-/- mice. INNOVATION AND
conclusionROS production stimulated by NoxO1 and p47phox limit endothelium-dependent relaxation and maintain blood pressure in mice. However, NoxO1 and p47phox cannot substitute each other despite their similar effect on vascular function. Deletion of NoxO1 induced an anti-inflammatory phenotype, whereas p47phox deletion rather elicited a hyper-inflammatory response.
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