Evidence map›Paper›PMID 27345301›Full record

ReviewCell and tissue research2016

Reactive oxygen species and fibrosis: further evidence of a significant liaison.

Kati Richter, Thomas Kietzmann

Abstract readReview
In one paragraph

Review in Cell and tissue research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed
–field-weighted citation impact
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

160 citing papers in PubMed.

  1. A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026
    Review
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  7. Fabry Disease: A Focus on the Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026
    Review
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  17. Polynucleotide HPTAntioxidants (Basel, Switzerland) · 2025
    Article
  18. Article
  19. Article
  20. Review

100 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.

Kati RichterFaculty of Biochemistry and Molecular Medicine and Biocenter Oulu, University of Oulu, Aapistie 7A, FI-90230, Oulu, Finland.
Thomas KietzmannFaculty of Biochemistry and Molecular Medicine and Biocenter Oulu, University of Oulu, Aapistie 7A, FI-90230, Oulu, Finland. tkietzm@gwdg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related diseases such as obesity, diabetes, non-alcoholic fatty liver disease, chronic kidney disease and cardiomyopathy are frequently associated with fibrosis. Work within the last decade has improved our understanding of the pathophysiological mechanisms contributing to fibrosis development. In particular, oxidative stress and the antioxidant system appear to be crucial modulators of processes such as transforming growth factor-β1 (TGF-β1) signalling, metabolic homeostasis and chronic low-grade inflammation, all of which play important roles in fibrosis development and persistence. In the current review, we discuss the connections between reactive oxygen species, antioxidant enzymes and TGF-β1 signalling, together with functional consequences, reflecting a concept of redox-fibrosis that can be targeted in future therapies. Graphical abstract ᅟ.

Indexed as

AnimalsEpigenesis, GeneticFibrosisHumansModels, BiologicalOxidative StressReactive Oxygen SpeciesTransforming Growth Factor beta1Reactive Oxygen SpeciesTransforming Growth Factor beta1AntioxidantsAntioxidative enzymesFibrosisMatrixReactive oxygen species (ROS)

Identifiers

PMID27345301
PMCPMC5010605

What OpenQuestion holds

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LicenceCC BY
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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.