Evidence map›Paper›PMID 24520085›Full record

ReviewReproductive sciences (Thousand Oaks, Calif.)2014

Advances in the Pathogenesis of Adhesion Development: The Role of Oxidative Stress.

Awoniyi O Awonuga, Jimmy Belotte, Suleiman Abuanzeh, Nicole M Fletcher, Michael P Diamond, Ghassan M Saed

Open access · greenAbstract readReview
In one paragraph

Review in Reproductive sciences (Thousand Oaks, Calif.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  5. Article
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  7. Article
  8. Peritendinous adhesion: Therapeutic targets and progress of drug therapy.Computational and structural biotechnology journal · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Is There a Genetic Predisposition to Postoperative Adhesion Development?Reproductive sciences (Thousand Oaks, Calif.) · 2021
    Review
  20. Review
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 2 institutions in 1 country.

Awoniyi O AwonugaDepartment of Obstetrics and Gynecology, CS Mott Center for Human Growth and Development, Wayne State University School of Medicine, Detroit, MI, USA Department of Obstetrics and Gynecology, Reproductive Endocrinology and Infertility, Wayne State University, School of Medicine, Detroit, MI, USA.
Jimmy BelotteDepartment of Obstetrics and Gynecology, CS Mott Center for Human Growth and Development, Wayne State University School of Medicine, Detroit, MI, USA.
Suleiman AbuanzehDepartment of Obstetrics and Gynecology, CS Mott Center for Human Growth and Development, Wayne State University School of Medicine, Detroit, MI, USA.
Nicole M FletcherDepartment of Obstetrics and Gynecology, CS Mott Center for Human Growth and Development, Wayne State University School of Medicine, Detroit, MI, USA.
Michael P DiamondDepartment of Obstetrics and Gynecology, Georgia Regents University, Augusta, GA, USA.
Ghassan M SaedDepartment of Obstetrics and Gynecology, CS Mott Center for Human Growth and Development, Wayne State University School of Medicine, Detroit, MI, USA Department of Obstetrics and Gynecology, Reproductive Endocrinology and Infertility, Wayne State University, School of Medicine, Detroit, MI, USA Department of Physiology, Program for Reproductive Sciences, Wayne State University, School of Medicine, Detroit, MI, USA Karmanos Cancer Institute, Molecular Biology and Genetics Program, Wayne State University School of Medicine, Detroit, MI, USA gsaed@med.wayne.edu.
Wayne State University · USAugusta University · US

Funding

DETROIT REPRODUCTIVE CAREER DEVELOPMENT RESEARCH CENTERK12HD001254 · NICHD · WAYNE STATE UNIVERSITY · PI HSU, CHAUR-DONG · 1999 to 2019
$4.8M
NICHD NIH HHS K12 HD001254
6 · The paper itself

Abstract

Over the past several years, there has been increasing recognition that pathogenesis of adhesion development includes significant contributions of hypoxia induced at the site of surgery, the resulting oxidative stress, and the subsequent free radical production. Mitochondrial dysfunction generated by surgically induced tissue hypoxia and inflammation can lead to the production of reactive oxygen and nitrogen species as well as antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase which when optimal have the potential to abrogate mitochondrial dysfunction and oxidative stress, preventing the cascade of events leading to the development of adhesions in injured peritoneum. There is a significant cross talk between the several processes leading to whether or not adhesions would eventually develop. Several of these processes present avenues for the development of measures that can help in abrogating adhesion formation or reformation after intraabdominal surgery.

Indexed as

adhesion markershypoxiaoxidative stresspostoperative adhesions

Identifiers

PMID24520085
PMCPMC4107571
OpenAlexW1982520218

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.