Evidence map›Paper›PMID 24122865›Full record

ReviewJournal of cellular biochemistry2014

Hydrogen peroxide as a damage signal in tissue injury and inflammation: murderer, mediator, or messenger?

Albert van der Vliet, Yvonne M W Janssen-Heininger

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

98 citing papers in PubMed, 230 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. [Advances in injectable and transdermal glucose-responsive insulin delivery systems].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Spatiotemporal HNature communications · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Review
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  18. Review
  19. Biofilm comes back: Controlling regrowth by mitigating the cell-matrix interaction.Chemical engineering journal (Lausanne, Switzerland : 1996) · 2025
    Article
  20. Review

38 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

2 authors at 1 institution in 1 country.

Albert van der VlietDepartment of Pathology, College of Medicine, University of Vermont, Burlington, Vermont, 05405.
Yvonne M W Janssen-Heininger
University of Vermont · US

Funding

REGULATION OF NFKB IN LUNG EPITHELIUM BY ROS/RNSR01HL060014 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI JANSSEN-HEININGER, YVONNE M. W. · 1999 to 2016
$5.9M
Dual Oxidase in Airway Epithelial Repair and RemodelingR01HL085646 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2008 to 2020
$4.7M
ENVIRONMENTAL PATHOLOGY TRAINING PROGRAMT32ES007122 · NIEHS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 1985 to 2012
$4.2M
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
TRANSLATIONAL RESEARCH IN LUNG BIOLOGY AND DISEASEP30RR031158 · NCRR · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI IRVIN, CHARLES G · 2010 to 2011
$2.6M
Cigarette Smoke-derived Electrophilic Aldehydes and Airway InflammationR01ES021476 · NIEHS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2012 to 2016
$1.9M
NCRR NIH HHS P30 RR031158NHLBI NIH HHS HL060014NHLBI NIH HHS R01 HL060014NHLBI NIH HHS R01 HL079331NHLBI NIH HHS R01 HL085646NIEHS NIH HHS ES021476NIEHS NIH HHS R01 ES021476NIEHS NIH HHS T32 ES007122NIEHS NIH HHS T32 ES07122‐30S1
6 · The paper itself

Abstract

Tissue injury and inflammation are associated with increased production of reactive oxygen species (ROS), which have the ability to induce oxidative injury to various biomolecules resulting in protein dysfunction, genetic instability, or cell death. However, recent observations indicate that formation of hydrogen peroxide (H2 O2 ) during tissue injury is also an essential feature of the ensuing wound healing response, and functions as an early damage signal to control several critical aspects of the wound healing process. Because innate oxidative wound responses must be tightly coordinated to avoid chronic inflammation or tissue injury, a more complete understanding is needed regarding the origins and dynamics of ROS production, and their critical biological targets. This prospect highlights the current experimental evidence implicating H2 O2 in early epithelial wound responses, and summarizes technical advances and approaches that may help distinguish its beneficial actions from its more deleterious actions in conditions of chronic tissue injury or inflammation.

Indexed as

Oxidative StressCell MovementChemotaxisCysteineHumansHydrogen PeroxideInflammationReactive Oxygen SpeciesSignal TransductionWound HealingCysteineHydrogen PeroxideReactive Oxygen SpeciesCELL MIGRATIONCHEMOTAXISCYSTEINENOX/DUOXREACTIVE OXYGEN SPECIESREDOX SIGNALING

Identifiers

PMID24122865
PMCPMC4363740
OpenAlexW1542007198

What OpenQuestion holds

Textmetadata
LicenceTDM
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.