Evidence map›Paper›PMID 27693992›Full record

ArticleRedox biology2016

The redox mechanism for vascular barrier dysfunction associated with metabolic disorders: Glutathionylation of Rac1 in endothelial cells.

Jingyan Han, Robert M Weisbrod, Di Shao, Yosuke Watanabe, Xiaoyan Yin, Markus M Bachschmid, Francesca Seta, Yvonne M W Janssen-Heininger, Reiko Matsui, Mengwei Zang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 56 citations in OpenAlex.

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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

12 authors at 4 institutions in 1 country.

Jingyan HanVascular Biology Section, Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA. Electronic address: jingyanh@bu.edu.
Robert M WeisbrodEvans Department of Medicine and the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Di ShaoVascular Biology Section, Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Yosuke WatanabeVascular Biology Section, Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Xiaoyan YinFramingham Heart Study, Boston University School of Medicine, Boston, MA, USA.
Markus M BachschmidVascular Biology Section, Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Francesca SetaVascular Biology Section, Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Yvonne M W Janssen-HeiningerDepartment of Pathology, University of Vermont College of Medicine, Burlington, VT, USA.
Reiko MatsuiVascular Biology Section, Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Mengwei ZangDepartment of Molecular Medicine, Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, South Texas Veterans Health Care System, San Antonio, TX, USA.
Naomi M HamburgEvans Department of Medicine and the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Richard A CohenVascular Biology Section, Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Boston University · USFramingham Heart Study · USThe University of Texas Health Science Center at San Antonio · USUniversity of Vermont · US

Funding

Redox-based Fas Signaling in Allergic Airway DiseaseR01HL079331 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI JANSSEN-HEININGER, YVONNE M. W. · 2005 to 2016
$4.2M
Redox Control of Hepatic Lipid MetabolismR01DK103750 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BACHSCHMID, MARKUS MICHAEL · 2015 to 2019
$1.8M
Regulation of ischemic limb vascularization by glutaredoxin-1R01HL133013 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MATSUI, REIKO · 2016 to 2019
$1.6M
Retinoic Acid Receptor, Lipid Metabolism, and Fatty Liver DiseaseR01DK100603 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ZANG, MENGWEI · 2015 to 2018
$1.5M
Alcohol-induced dysregulation of thiol homeostasis and endothelial functionR21AA026922 · NIAAA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAN, JINGYAN, ZANG, MENGWEI · 2019 to 2020
$439k
mTORC1 activation and alcoholic liver injuryR21AA021181 · NIAAA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ZANG, MENGWEI · 2013 to 2014
$421k
NHLBI NIH HHS R01 HL079331NHLBI NIH HHS R01 HL133013NIAAA NIH HHS R21 AA021181NIAAA NIH HHS R21 AA026922NIDDK NIH HHS R01 DK100603NIDDK NIH HHS R01 DK103750
6 · The paper itself

Abstract

backgroundOxidative stress is implicated in increased vascular permeability associated with metabolic disorders, but the underlying redox mechanism is poorly defined. S-glutathionylation, a stable adduct of glutathione with protein sulfhydryl, is a reversible oxidative modification of protein and is emerging as an important redox signaling paradigm in cardiovascular physiopathology. The present study determines the role of protein S-glutathionylation in metabolic stress-induced endothelial cell permeability. METHODS AND

resultsIn endothelial cells isolated from patients with type-2 diabetes mellitus, protein S-glutathionylation level was increased. This change was also observed in aortic endothelium in ApoE deficient (ApoE

conclusionsGlutathionylation and inactivation of Rac1 in endothelial cells represent a novel redox mechanism of vascular barrier dysfunction associated with metabolic disorders.

Indexed as

Oxidation-ReductionAnimalsAortaApolipoproteins ECapillary PermeabilityCell LineCysteineEndothelial CellsEndothelium, VascularGene ExpressionGlutaredoxinsGlutathioneHumansMaleMetabolic DiseasesMiceApolipoproteins ECysteineGlrx protein, mouseGlutaredoxinsGlutathionerac1 GTP-Binding ProteinActin cytoskeletonApoE-deficient miceEndothelial barrier functionGlutaredoxin-1Protein S-glutathionylationSmall Rho GTPase Rac1

Identifiers

PMID27693992
PMCPMC5045950
OpenAlexW2519539563

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.