Evidence map›Paper›PMID 21300668›Full record

ArticleHypertension (Dallas, Tex. : 1979)2011

Equol-stimulated mitochondrial reactive oxygen species activate endothelial nitric oxide synthase and redox signaling in endothelial cells: roles for F-actin and GPR30.

David J Rowlands, Sarah Chapple, Richard C M Siow, Giovanni E Mann

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

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  11. The gut microbiome as a modulator of arterial function and age-related arterial dysfunction.American journal of physiology. Heart and circulatory physiology · 2024
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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

4 authors at 1 institution in 1 country.

David J RowlandsCardiovascular Division, British Heart Foundation Centre for Research Excellence, School of Medicine, Franklin-Wilkins Building (Room 3.01), King's College London, 150 Stamford St, London SE1 9NH, UK.
Sarah Chapple
Richard C M Siow
Giovanni E Mann
British Heart Foundation · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/S/K/2004/11207British Heart Foundation FS/1999075/11799British Heart Foundation FS/99075
6 · The paper itself

Abstract

We reported previously that dietary isoflavones modulate arterial blood pressure in vivo and that the daidzein metabolite equol rapidly activates endothelial NO synthase (eNOS) via Akt and extracellular signal-regulated kinase 1/2-dependent signaling. In this study, we report the first evidence in human endothelial cells that acute stimulation of mitochondrial superoxide generation by equol (100 nmol/L) is required for eNOS activation. Scavengers of superoxide (superoxide dismutase and manganese [III] tetrakis[1-methyl-4-pyridyl]porphyrin) abrogated equol stimulated Akt and eNOS phosphorylation, and the mitochondrial complex I inhibitor rotenone inhibited Akt, extracellular signal-regulated kinase 1/2, and eNOS phosphorylation, as well as NO-mediated increases in intracellular cGMP. Equol also induced rapid alterations in F-actin fiber distribution, with depolymerization of F-actin with cytochalasin D abrogating equol-stimulated mitochondrial superoxide generation. Treatment of cells with pertussis toxin or inhibition of GPR30/epidermal growth factor receptor kinase transactivation prevented equol-induced activation of extracellular signal-regulated kinase 1/2 via c-Src, Akt, and eNOS. Moreover, inhibition of epidermal growth factor receptor kinase activation with AG-1478 abrogated equol-stimulated mitochondrial reactive oxygen species generation and subsequent kinase and eNOS activation. Our findings suggest that equol-stimulated mitochondrial reactive oxygen species modulate endothelial redox signaling and NO release involving transactivation of epidermal growth factor receptor kinase and reorganization of the F-actin cytoskeleton. Identification of these novel actions of equol may provide valuable insights for therapeutic strategies to restore endothelial function in cardiovascular disease.

Indexed as

ActinsAnalysis of VarianceCells, CulturedEndothelial CellsEquolErbB ReceptorsHumansIsoflavonesMitochondriaNitric Oxide Synthase Type IIIOxidation-ReductionPhytoestrogensReactive Oxygen SpeciesReceptors, EstrogenReceptors, G-Protein-CoupledSignal Transduction4',7-dihydroxy-3,4-dihydroisoflavoneActinsEquolErbB ReceptorsGPER1 protein, humanIsoflavonesNitric Oxide Synthase Type IIIPhytoestrogensReactive Oxygen SpeciesReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID21300668
PMCPMC3086276
OpenAlexW2150897767

What OpenQuestion holds

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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.