Evidence map›Paper›PMID 31210841›Full record

ReviewOxidative medicine and cellular longevity2019

Glutathione "Redox Homeostasis" and Its Relation to Cardiovascular Disease.

Vladan P Bajic, Christophe Van Neste, Milan Obradovic, Sonja Zafirovic, Djordje Radak, Vladimir B Bajic, Magbubah Essack, Esma R Isenovic

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
10.8field-weighted citation impact, top 1% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Review
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  6. Use of Human Serum Albumin CysAntioxidants (Basel, Switzerland) · 2026
    Review
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  13. Cytoprotective Potential ofInternational journal of molecular sciences · 2025
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  18. Review
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25 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Vladan P BajicLaboratory for Radiobiology and Molecular Genetics, Institute of Nuclear Sciences Vinca, University of Belgrade, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia.
Christophe Van NesteKing Abdullah University of Science and Technology (KAUST), Computational Bioscience Research Center (CBRC), Thuwal 23955-6900, Saudi Arabia.
Milan ObradovicLaboratory for Radiobiology and Molecular Genetics, Institute of Nuclear Sciences Vinca, University of Belgrade, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia.
Sonja ZafirovicLaboratory for Radiobiology and Molecular Genetics, Institute of Nuclear Sciences Vinca, University of Belgrade, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia.ORCID 0000-0002-5486-0079
Djordje RadakDepartment of Vascular Surgery, Dedinje Cardiovascular Institute, Belgrade University School of Medicine, Belgrade, Serbia.
Vladimir B BajicKing Abdullah University of Science and Technology (KAUST), Computational Bioscience Research Center (CBRC), Thuwal 23955-6900, Saudi Arabia.ORCID 0000-0001-5435-4750
Magbubah EssackKing Abdullah University of Science and Technology (KAUST), Computational Bioscience Research Center (CBRC), Thuwal 23955-6900, Saudi Arabia.ORCID 0000-0003-2709-5356
Esma R IsenovicLaboratory for Radiobiology and Molecular Genetics, Institute of Nuclear Sciences Vinca, University of Belgrade, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia.ORCID 0000-0002-0012-2636
University of Belgrade · RSKing Abdullah University of Science and Technology · SAInstitute for Cardiovascular Diseases of Vojvodina · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired "redox homeostasis," which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.

Indexed as

Oxidative StressSignal TransductionAnimalsCardiovascular DiseasesGlutathioneHumansGlutathione

Identifiers

PMID31210841
PMCPMC6532282
OpenAlexW2944278437

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.