Evidence map›Paper›PMID 39724463›Full record

ReviewClinical and translational medicine2025

Intestinal oxygen utilisation and cellular adaptation during intestinal ischaemia-reperfusion injury.

Paraschos Archontakis-Barakakis, Theodoros Mavridis, David-Dimitris Chlorogiannis, Georgios Barakakis, Eleni Laou, Daniel I Sessler, George Gkiokas, Athanasios Chalkias

Abstract readReview
In one paragraph

Review in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Curcumin in ischemia-reperfusion injury across multiple organs: A review.The Journal of international medical research · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Interplay between volemic balance and the intestinal tract: insights on biomarkers and diagnostic tests used to assess intestinal morphofunctional barrier.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
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

8 authors.

Paraschos Archontakis-BarakakisDepartment of Medicine, Redington-Fairview General Hospital, Skowhegan, Maine, USA.
Theodoros MavridisDepartment of Neurology, Tallaght University Hospital (TUH)/The Adelaide and Meath Hospital incorporating the National Children's Hospital (AMNCH), Dublin, Ireland.
David-Dimitris ChlorogiannisDepartment of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Georgios BarakakisFaculty of Health Sciences, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Eleni LaouDepartment of Anesthesiology, Agia Sophia Children's Hospital, Athens, Greece.
Daniel I SesslerCenter for Outcomes Research and Department of Anesthesiology, UTHealth, Houston, Texas, USA.
George GkiokasSecond Department of Surgery, Aretaieion University Hospital, National and Kapodistrian University of Athens, Athens, Greece.
Athanasios ChalkiasOutcomes Research Consortium®, Houston, Texas, USA.ORCID 0000-0002-7634-4665

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gastrointestinal tract can be deranged by ailments including sepsis, trauma and haemorrhage. Ischaemic injury provokes a common constellation of microscopic and macroscopic changes that, together with the paradoxical exacerbation of cellular dysfunction and death following restoration of blood flow, are collectively known as ischaemia-reperfusion injury (IRI). Although much of the gastrointestinal tract is normally hypoxemic, intestinal IRI results when there is inadequate oxygen availability due to poor supply (pathological hypoxia) or abnormal tissue oxygen use and metabolism (dysoxia). Intestinal oxygen uptake usually remains constant over a wide range of blood flows and pressures, with cellular function being substantively compromised when ischaemia leads to a >50% decline in intestinal oxygen consumption. Restoration of perfusion and oxygenation provokes additional injury, resulting in mucosal damage and disruption of intestinal barrier function. The primary cellular mechanism for sensing hypoxia and for activating a cascade of cellular responses to mitigate the injury is a family of heterodimer proteins called hypoxia-inducible factors (HIFs). The HIF system is connected to numerous biochemical and immunologic pathways induced by IRI and the concentration of those proteins increases during hypoxia and dysoxia. Activation of the HIF system leads to augmented transcription of specific genes in various types of affected cells, but may also augment apoptotic and inflammatory processes, thus aggravating gut injury. KEY POINTS: During intestinal ischaemia, mitochondrial oxygen uptake is reduced when cellular oxygen partial pressure decreases to below the threshold required to maintain normal oxidative metabolism. Upon reperfusion, intestinal hypoxia may persist because microcirculatory flow remains impaired and/or because available oxygen is consumed by enzymes, intestinal cells and neutrophils.

Indexed as

Intestinal MucosaOxygenReperfusion InjuryAdaptation, PhysiologicalAnimalsHumansOxygen ConsumptionOxygendysoxiahypoxiaintestineischaemia–reperfusion injuryoxygen

Identifiers

PMID39724463
PMCPMC11670310

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.