Evidence map›Paper›PMID 42890525›Full record

ArticleFrontiers in endocrinology2026

NADPH oxidase 4 as a source of hydrogen peroxide can regulate norepinephrine levels and vascular contraction.

Heike Brendel, Jennifer Mittag, Nicole Bechmann, Amna Shahid Mehmood-Ashraf, Antje Schauer, Patrick Diaba-Nuhoho, Mirko Peitzsch, Graeme Eisenhofer, Stefan R Bornstein, Henning Morawietz and 1 more

Abstract read
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In one paragraph

Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Heike BrendelDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Jennifer MittagDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Nicole BechmannInstitute for Clinical Chemistry and Laboratory Medicine, University Hospital Carl Gustav Carus, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Amna Shahid Mehmood-AshrafDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Antje SchauerDepartment of Internal Medicine and Cardiology, Heart Center Dresden - Laboratory of Experimental and Molecular Cardiology, Technische Universität Dresden, Dresden, Germany.
Patrick Diaba-NuhohoDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Mirko PeitzschInstitute for Clinical Chemistry and Laboratory Medicine, University Hospital Carl Gustav Carus, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Graeme EisenhoferDepartment of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Stefan R BornsteinDepartment of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Henning MorawietzDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Coy BrunssenDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The adrenal glands play a pivotal role in maintaining physiological homeostasis, and disturbance in their function can lead to significant clinical disorders, including hypertension, and adrenal insufficiency. Reactive oxygen species (ROS), once considered merely byproducts of cellular metabolism, are now recognized as critical signaling molecules within the adrenal cortex and medulla. Among the major enzymatic sources of ROS are NADPH oxidases (Nox). Dysregulation of Nox-derived ROS has been linked to altered steroidogenesis, oxidative stress- mediated adrenal damage, and tumorigenic processes. We aimed to elucidate the role of Nox4 on adrenal function under healthy conditions. Methods: Using Nox4-knockout mouse model, adrenal effects were assessed by histological analysis, real-time PCR, and cathecholamine quantification using HPLC-ECD and LC-MS/MS. Cardiovascular function was evaluated by echocardiography, blood pressure measurements, and ex vivo vascular function analysis. Results: Here, we demonstrated that Nox4 is expressed in the mouse adrenal gland, and its deletion led to decreased hydrogen peroxide production, diminished dopamine beta-hydroxylase mRNA expression, and reduced norepinephrine levels. In chromaffin cells, treatment with hydrogen peroxide stimulated catecholamine release and increased dopamine beta-hydroxylase expression, indicating a regulatory role of hydrogen peroxide in catecholamine synthesis and secretion. Further analysis of the physiological consequences of reduced norepinephrine levels in Nox4 Conclusion: Our findings provide evidence that Nox4-derived H

Indexed as

Hydrogen PeroxideNADPH Oxidase 4NorepinephrineVasoconstrictionAdrenal GlandsAnimalsChromaffin CellsMaleMiceMice, Inbred C57BLMice, KnockoutReactive Oxygen SpeciesHydrogen PeroxideNADPH Oxidase 4NorepinephrineNox4 protein, mouseReactive Oxygen Speciesadrenaladrenergic receptorcatecholaminesNADPH oxidase 4vascular contraction

Identifiers

PMID42890525
PMCPMC13671950

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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.