Evidence map›Paper›PMID 33541847›Full record

ReviewRedox biology2021

Redox-related biomarkers in human cardiovascular disease - classical footprints and beyond.

Andreas Daiber, Omar Hahad, Ioanna Andreadou, Sebastian Steven, Steffen Daub, Thomas Münzel

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
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  15. Article
  16. Electrochemistry as a Tool for Redox-Based Bio-Information Processing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  17. Article
  18. Article
  19. Review
  20. GSTP1 inhibits angiotensin II-induced atrial fibrillation by regulating ferroptosis.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025
    Article

4 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

6 authors at 4 institutions in 2 countries.

Andreas DaiberDepartment of Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Langenbeckstr. 1, 55131, Mainz, Germany. Electronic address: daiber@uni-mainz.de.
Omar HahadDepartment of Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Langenbeckstr. 1, 55131, Mainz, Germany.
Ioanna AndreadouLaboratory of Pharmacology, Faculty of Pharmacy, National and Kapodistrian University of Athens, Athens, Greece.
Sebastian StevenDepartment of Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany.
Steffen DaubDepartment of Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany.
Thomas MünzelDepartment of Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Langenbeckstr. 1, 55131, Mainz, Germany. Electronic address: tmuenzel@uni-mainz.de.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEGerman Centre for Cardiovascular Research · DENational and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Global epidemiological studies show that chronic non-communicable diseases such as atherosclerosis and metabolic disorders represent the leading cause of premature mortality and morbidity. Cardiovascular disease such as ischemic heart disease is a major contributor to the global burden of disease and the socioeconomic health costs. Clinical and epidemiological data show an association of typical oxidative stress markers such as lipid peroxidation products, 3-nitrotyrosine or oxidized DNA/RNA bases with all major cardiovascular diseases. This supports the concept that the formation of reactive oxygen and nitrogen species by various sources (NADPH oxidases, xanthine oxidase and mitochondrial respiratory chain) represents a hallmark of the leading cardiovascular comorbidities such as hyperlipidemia, hypertension and diabetes. These reactive oxygen and nitrogen species can lead to oxidative damage but also adverse redox signaling at the level of kinases, calcium handling, inflammation, epigenetic control, circadian clock and proteasomal system. The in vivo footprints of these adverse processes (redox biomarkers) are discussed in the present review with focus on their clinical relevance, whereas the details of their mechanisms of formation and technical aspects of their detection are only briefly mentioned. The major categories of redox biomarkers are summarized and explained on the basis of suitable examples. Also the potential prognostic value of redox biomarkers is critically discussed to understand what kind of information they can provide but also what they cannot achieve.

Indexed as

Cardiovascular DiseasesBiomarkersHumansNADPH OxidasesOxidation-ReductionOxidative StressReactive Oxygen SpeciesBiomarkersNADPH OxidasesReactive Oxygen SpeciesCardiovascular diseaseComorbiditiesOxidative stressRedox biomarker

Identifiers

PMID33541847
PMCPMC8113038
OpenAlexW3123087664

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.