Evidence map›Paper›PMID 18508729›Full record

ArticleFrontiers in bioscience : a journal and virtual library2008

Oxidative stress-induced disruption of epithelial and endothelial tight junctions.

Radhakrishna Rao

Abstract read
In one paragraph

Article in Frontiers in bioscience : a journal and virtual library, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed, 1 pooled it
–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

200 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. The oxidative stress paradigm in arbovirus infections: mechanisms and therapeutic insights.Redox report : communications in free radical research · 2026
    Review
  3. Article
  4. Review
  5. Article
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  7. Article
  8. Article
  9. Article
  10. A Sea Buckthorn Pomace Polysaccharide Mitigates HFoods (Basel, Switzerland) · 2026
    Article
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  12. Review
  13. Article
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  15. Article
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  17. Article
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140 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

1 author.

Radhakrishna RaoDepartment of Physiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA. rkrao@physio1.utmem.edu

Funding

INTESTINAL MUCOSAL PROTECTION BY EPIDERMAL GROWTH FACTORR01DK055532 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, RADHAKRISHNA · 1998 to 2020
$4.7M
MECHANISM OF ENDOTOXIN ABSORPTION IN ALCOHOLISMR01AA012307 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, RADHAKRISHNA · 2000 to 2014
$3.9M
Intestinal Mucosal Protection by Epidermal Growth FactorR56DK055532 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, RADHAKRISHNA · 2009 to 2009
$345k
NIAAA NIH HHS AA12307NIAAA NIH HHS R01 AA012307NIDDK NIH HHS DK55532NIDDK NIH HHS R01 DK055532
6 · The paper itself

Abstract

Mounting body of evidence indicates that the disruption of epithelial tight junctions and resulting loss of barrier function play a crucial role in the pathogenesis of a variety of gastrointestinal, hepatic, pulmonary, kidney and ocular diseases. Increased production of inflammatory mediators such as cytokines and reactive oxygen species disrupt the epithelial and endothelial barrier function by destabilizing tight junctions. Oxidative stress induced by various reactive oxygen species such as hydrogen peroxide, nitric oxide, peroxynitrite and hypochlorous acid disrupt the epithelial and endothelial tight junctions in various tissues. The mechanism involved in oxidative stress-induced disruption of tight junction includes protein modification such as thiol oxidation, phosphorylation, nitration and carbonylation. The role of signaling molecules such as protein kinases and protein phosphatases in regulation of tight junctions is discussed in this article. Understanding such mechanisms in oxidative stress-induced disruption of epithelial and endothelial barrier functions is likely to provide insight into the pathogenesis of various inflammatory diseases, and may form a basis for the design of treatment strategies for different diseases.

Indexed as

ActinsCaco-2 CellsEndothelial CellsEpithelial CellsExtracellular Signal-Regulated MAP KinasesGlutathioneGlutathione DisulfideHumansHydrogen PeroxideNitric OxideOxidative StressPeroxynitrous AcidSignal TransductionSulfhydryl CompoundsTight JunctionsActinsExtracellular Signal-Regulated MAP KinasesGlutathioneGlutathione DisulfideHydrogen PeroxideNitric OxidePeroxynitrous AcidSulfhydryl Compounds

Identifiers

PMID18508729
PMCPMC6261932

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.