Evidence map›Paper›PMID 32948023›Full record

ReviewInternational journal of molecular sciences2020

Role of Glutaredoxin-1 and Glutathionylation in Cardiovascular Diseases.

Mannix Burns, Syed Husain Mustafa Rizvi, Yuko Tsukahara, David R Pimentel, Ivan Luptak, Naomi M Hamburg, Reiko Matsui, Markus M Bachschmid

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

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  14. Emerging chemistry and biology in protein glutathionylation.Current opinion in chemical biology · 2022
    Review
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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

8 authors at 1 institution in 1 country.

Mannix BurnsVascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, 650 Albany St., Boston, MA 02118, USA.ORCID 0000-0001-6091-3010
Syed Husain Mustafa RizviVascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, 650 Albany St., Boston, MA 02118, USA.
Yuko TsukaharaVascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, 650 Albany St., Boston, MA 02118, USA.
David R PimentelCardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, 650 Albany St., Boston, MA 02118, USA.
Ivan LuptakCardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, 650 Albany St., Boston, MA 02118, USA.ORCID 0000-0001-7498-7694
Naomi M HamburgVascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, 650 Albany St., Boston, MA 02118, USA.
Reiko MatsuiVascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, 650 Albany St., Boston, MA 02118, USA.
Markus M BachschmidVascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, 650 Albany St., Boston, MA 02118, USA.
Boston University · US

Funding

Mitochondrial Dynamics and UCP2 - Endothelial Dysfunction in Human ObesityR01HL115391 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAMBURG, NAOMI MIRIAM · 2013 to 2017
$2.8M
Regulation of ischemic limb vascularization by glutaredoxin-1R01HL133013 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MATSUI, REIKO · 2016 to 2019
$1.6M
Regulation of ischemic vascularization by glutaredoxin-1 by agingR03AG051857 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MATSUI, REIKO · 2016 to 2017
$236k
American Heart Association 16GRNT27660006NHLBI NIH HHS R01 HL115391NHLBI NIH HHS R01 HL133013NIH HHS 1UL1TR001430NIH HHS R01 HL133013, R01 D K103750NIH HHS R03 AG 051857
6 · The paper itself

Abstract

Cardiovascular diseases are the leading cause of death worldwide, and as rates continue to increase, discovering mechanisms and therapeutic targets become increasingly important. An underlying cause of most cardiovascular diseases is believed to be excess reactive oxygen or nitrogen species. Glutathione, the most abundant cellular antioxidant, plays an important role in the body's reaction to oxidative stress by forming reversible disulfide bridges with a variety of proteins, termed glutathionylation (GSylation). GSylation can alter the activity, function, and structure of proteins, making it a major regulator of cellular processes. Glutathione-protein mixed disulfide bonds are regulated by glutaredoxins (Glrxs), thioltransferase members of the thioredoxin family. Glrxs reduce GSylated proteins and make them available for another redox signaling cycle. Glrxs and GSylation play an important role in cardiovascular diseases, such as myocardial ischemia and reperfusion, cardiac hypertrophy, peripheral arterial disease, and atherosclerosis. This review primarily concerns the role of GSylation and Glrxs, particularly glutaredoxin-1 (Glrx), in cardiovascular diseases and the potential of Glrx as therapeutic agents.

Indexed as

Protein Processing, Post-TranslationalAnimalsAntioxidantsCardiovascular DiseasesCysteineDisulfidesEndothelial CellsGlucoseGlutaredoxinsGlutathioneHomeostasisHumansLipid MetabolismMiceMice, KnockoutMyocytes, CardiacAntioxidantsCysteinecysteine thiolateDisulfidesGlucoseGlutaredoxinsGlutathioneReactive Nitrogen SpeciesReactive Oxygen Speciescardiovascular diseaseglutaredoxinglutathionylationredox signaling

Identifiers

PMID32948023
PMCPMC7555996
OpenAlexW3085565522

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.