Evidence map›Paper›PMID 30576919›Full record

ArticleRedox biology2019

NOXA1-dependent NADPH oxidase regulates redox signaling and phenotype of vascular smooth muscle cell during atherogenesis.

Aleksandr E Vendrov, Arihiro Sumida, Chandrika Canugovi, Andrey Lozhkin, Takayuki Hayami, Nageswara R Madamanchi, Marschall S Runge

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% of its field
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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape.Journal of the American Heart Association · 2020
    Pooled it
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  3. Aging-AssociatedJournal of the American Heart Association · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Aleksandr E VendrovFrankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Arihiro SumidaFrankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Chandrika CanugoviFrankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Andrey LozhkinFrankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Takayuki HayamiFrankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Nageswara R MadamanchiFrankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Marschall S RungeFrankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: mrunge@med.umich.edu.
University of Michigan–Ann Arbor · US

Funding

Michigan Mouse Metabolic Phenotyping CenterU2CDK110768 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELIAS, CAROL FUZETI · 2016 to 2021
$6.2M
Nox1/NoxA1 Regulation of Vascular Reactivity and Sodium Excretion in Health and Hypertension.R01HL139842 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ARENDSHORST, WILLIAM J, MADAMANCHI, NAGESWARA R · 2018 to 2021
$2.9M
Molecular Characterization of NoxA1 in VSMC NADPH Oxidase ActivationR01HL111664 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RUNGE, MARSCHALL S. · 2012 to 2015
$1.5M
NHLBI NIH HHS R01 HL111664NHLBI NIH HHS R01 HL139842NIDDK NIH HHS U2C DK110768
6 · The paper itself

Abstract

Increased reactive oxygen species (ROS) production and inflammation are key factors in the pathogenesis of atherosclerosis. We previously reported that NOX activator 1 (NOXA1) is the critical functional homolog of p67phox for NADPH oxidase activation in mouse vascular smooth muscle cells (VSMC). Here we investigated the effects of systemic and SMC-specific deletion of Noxa1 on VSMC phenotype during atherogenesis in mice. Neointimal hyperplasia following endovascular injury was lower in Noxa1-deficient mice versus the wild-type following endovascular injury. Noxa1 deletion in Apoe

Indexed as

Oxidation-ReductionSignal TransductionAdaptor Proteins, Signal TransducingAnimalsApolipoproteins EAtherosclerosisBiomarkersEnzyme ActivationGene DeletionGenetic LociKruppel-Like Factor 4MiceMice, KnockoutMice, TransgenicMuscle, Smooth, VascularMyocytes, Smooth MuscleAdaptor Proteins, Signal TransducingApolipoproteins EBiomarkersKlf4 protein, mouseKruppel-Like Factor 4NADPH OxidasesNoxa1 protein, mouseProteinsReactive Oxygen SpeciesReceptors, LDLTumor Necrosis Factor-alphaAtherosclerosisKLF4Macrophage-like cellsNOXA1Oxidative stressSmooth muscle cells

Identifiers

PMID30576919
PMCPMC6302039
OpenAlexW2902330407

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.