ArticleCirculation2017
Distinct Regulatory Effects of Myeloid Cell and Endothelial Cell NAPDH Oxidase 2 on Blood Pressure.
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Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44citing papers in PubMed
4.8field-weighted citation impact, top 4% of its field
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44 citing papers in PubMed, 61 citations in OpenAlex.
- Renin-Angiotensin Signaling and Vascular Function: Insights into Health and Disease.Acta physiologica (Oxford, England) · 2026Review
- Neutrophil NADPH oxidase breaks the inflammatory IL-1β/IL-17A circuit to enhance pathogen clearance during respiratory virus infections.Nature communications · 2026Article
- Skeletal muscle knockout of NAD(P)H oxidase 2 delays the development of isotonic diaphragm fatigue in mice.Free radical biology & medicine · 2025Article
- Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025Review
- TET2 has endothelial-specific roles in interferon responses that are dysregulated by hyperglycemia in vitro and in vivo.The Journal of biological chemistry · 2025Article
- Epigenetic Regulation of Innate and Adaptive Immune Cells in Salt-Sensitive Hypertension.Circulation research · 2025Review
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
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- Single-Cell RNA-Seq Reveals Coronary Heterogeneity and Identifies CD133Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Factors influencing new-onset hypertension in elderly patients with obstructive sleep apnea: A multicenter cohort study.Clinical and translational science · 2023Article
- GSK3 as a Master Regulator of Cellular Processes.International journal of molecular sciences · 2023Article
- Deficiency of endothelial sirtuin1 in mice stimulates skeletal muscle insulin sensitivity by modifying the secretome.Nature communications · 2023Article
- Bedding as a variable affecting fasting blood glucose and vascular physiology in mice.American journal of physiology. Heart and circulatory physiology · 2023Article
- Skeletal muscle Nox4 knockout prevents and Nox2 knockout blunts loss of maximal diaphragm force in mice with heart failure with reduced ejection fraction.Free radical biology & medicine · 2023Article
- Genetic Modifications to Alter Blood Pressure Level.Biomedicines · 2022Review
- Nox2 underpins microvascular inflammation and vascular contributions to cognitive decline.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Targeting the ASMase/S1P pathway protects from sortilin-evoked vascular damage in hypertension.The Journal of clinical investigation · 2022Article
- Phytochemical‑rich herbal formula ATG‑125 protects against sucrose‑induced gastrocnemius muscle atrophy by rescuing Akt signaling and improving mitochondrial dysfunction in young adult mice.Molecular medicine reports · 2022Article
- Enhanced Heart Failure in Redox-Dead Cys17Ser PKARIα Knock-In Mice.Journal of the American Heart Association · 2021Article
- Nox2-deficient Tregs improve heart transplant outcomes via their increased graft recruitment and enhanced potency.JCI insight · 2021Article
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Authors and funding
17 authors at 1 institution in 1 country.
Can Martin SagFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Moritz SchnelleFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Juqian ZhangFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Colin E MurdochFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Sabine KossmannFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Andrea ProttiFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Celio X C SantosFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Greta SawyerFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Xiaohong ZhangFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Heloise Mongue-DinFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Daniel A RichardsFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Alison C BrewerFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Oleksandra PrysyazhnaFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Lars S MaierFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Philip WenzelFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Philip J EatonFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.).
Ajay M ShahFrom King's College London British Heart Foundation Centre of Excellence, Cardiovascular Division, United Kingdom (C.M.S., M.S., J.Z., C.E.M., A.P., C.X.C.S., G.S., X.Z., H.M.-D., D.A.R., A.C.B., A.P., P.J.E., A.M.S.); Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany (C.M.S., L.S.M.); Department of Cardiology and Pneumology, Medical Center Goettingen, Germany (M.S.); and Center for Cardiology and Center for Thrombosis and Hemostasis, University Medical Center Mainz, Germany (S.K., P.W.). ajay.shah@kcl.ac.uk.
Nephrologisches Zentrum Goettingen · DE
Funding
British Heart Foundation PG/08/110/26228British Heart Foundation PG/15/119/31970British Heart Foundation PG/15/27/31374British Heart Foundation RG/13/11/30384
Abstract
backgroundHypertension caused by increased renin-angiotensin system activation is associated with elevated reactive oxygen species production. Previous studies implicate NADPH oxidase (Nox) proteins as important reactive oxygen species sources during renin-angiotensin system activation, with different Nox isoforms being potentially involved. Among these, Nox2 is expressed in multiple cell types, including endothelial cells, fibroblasts, immune cells, and microglia. Blood pressure (BP) is regulated at the central nervous system, renal, and vascular levels, but the cell-specific role of Nox2 in BP regulation is unknown.
methodsWe generated a novel mouse model with a floxed Nox2 gene and used Tie2-Cre, LysM Cre, or Cdh5-CreERT2 driver lines to develop cell-specific models of Nox2 perturbation to investigate its role in BP regulation.
resultsUnexpectedly, Nox2 deletion in myeloid but not endothelial cells resulted in a significant reduction in basal BP. Both Tie2-CreNox2 knockout (KO) mice (in which Nox2 was deficient in both endothelial cells and myeloid cells) and LysM CreNox2KO mice (in which Nox2 was deficient in myeloid cells) had significantly lower BP than littermate controls, whereas basal BP was unaltered in Cdh5-CreERT2 Nox2KO mice (in which Nox2 is deficient only in endothelial cells). The lower BP was attributable to an increased NO bioavailability that dynamically dilated resistance vessels in vivo under basal conditions without a change in renal function. Myeloid-specific Nox2 deletion had no effect on angiotensin II-induced hypertension, which, however, was blunted in Tie2-CreNox2KO mice, along with preservation of endothelium-dependent relaxation during angiotensin II stimulation.
conclusionsWe identify a hitherto unrecognized modulation of basal BP by myeloid cell Nox2, whereas endothelial cell Nox2 regulates angiotensin II-induced hypertension. These results identify distinct cell-specific roles for Nox2 in BP regulation.
Indexed as
Angiotensin IIAnimalsBlood PressureElectron Spin Resonance SpectroscopyEndothelial CellsHypertensionMaleMembrane GlycoproteinsMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMyeloid CellsNADPH Oxidase 2NADPH OxidasesAngiotensin IICybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH Oxidasesangiotensin IIblood pressuremiceNADPH oxidase
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