Evidence map›Paper›PMID 23305298›Full record

ReviewAntioxidants & redox signaling2013

Inflammatory bowel disease: mechanisms, redox considerations, and therapeutic targets.

Fiorella Biasi, Gabriella Leonarduzzi, Patricia I Oteiza, Giuseppe Poli

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 2 pooled it
10.0field-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

134 citing papers in PubMed, 2 syntheses or guidelines pooled it, 285 citations in OpenAlex.

  1. Debate on the relationship betweenFrontiers in microbiology · 2024
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  16. De novo DUOX2 expression in neutrophil subsets shapes the pathogenesis of intestinal disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  18. Article
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74 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

4 authors at 3 institutions in 2 countries.

Fiorella Biasi1 Department of Clinical and Biological Sciences, University of Turin , San Luigi Gonzaga Hospital, Orbassano, Italy .
Gabriella Leonarduzzi
Patricia I Oteiza
Giuseppe Poli
Ospedale San Luigi Gonzaga · ITUniversity of California, Davis · USUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is thought to play a key role in the development of intestinal damage in inflammatory bowel disease (IBD), because of its primary involvement in intestinal cells' aberrant immune and inflammatory responses to dietary antigens and to the commensal bacteria. During the active disease phase, activated leukocytes generate not only a wide spectrum of pro-inflammatory cytokines, but also excess oxidative reactions, which markedly alter the redox equilibrium within the gut mucosa, and maintain inflammation by inducing redox-sensitive signaling pathways and transcription factors. Moreover, several inflammatory molecules generate further oxidation products, leading to a self-sustaining and auto-amplifying vicious circle, which eventually impairs the gut barrier. The current treatment of IBD consists of long-term conventional anti-inflammatory therapy and often leads to drug refractoriness or intolerance, limiting patients' quality of life. Immune modulators or anti-tumor necrosis factor α antibodies have recently been used, but all carry the risk of significant side effects and a poor treatment response. Recent developments in molecular medicine point to the possibility of treating the oxidative stress associated with IBD, by designing a proper supplementation of specific lipids to induce local production of anti-inflammatory derivatives, as well as by developing biological therapies that target selective molecules (i.e., nuclear factor-κB, NADPH oxidase, prohibitins, or inflammasomes) involved in redox signaling. The clinical significance of oxidative stress in IBD is now becoming clear, and may soon lead to important new therapeutic options to lessen intestinal damage in this disease.

Indexed as

AnimalsAnti-Inflammatory AgentsHumansInflammatory Bowel DiseasesOxidation-ReductionOxidative StressAnti-Inflammatory Agents

Identifiers

PMID23305298
PMCPMC3809610
OpenAlexW1988581085

What OpenQuestion holds

Textmetadata
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.