Evidence map›Paper›PMID 31985456›Full record

ArticleClinical hemorheology and microcirculation2020

Does ischemic preconditioning increase flap survival by ADORA2B receptor activation?

Pinar Ulker, Ozlenen Ozkan, Matteo Amoroso, Mutay Aslan, Ibrahim Bassorgun, Mehmet Can Ubur, Kerim Ünal, Filiz Ozcan, Omer Ozkan

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Clinical hemorheology and microcirculation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
4 · The record

Corrections and comments

  • Retraction · 2025-11-23Compromised Peer Review · Concerns/Issues about Referencing/Attributions · Concerns/Issues about Third Party Involvement · Investigation by Journal/Publisher · · See also: https://pubpeer.com/publications/5217AF81AE9A7E314BA35F5D87B893
  • Retracted
5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Pinar UlkerDepartment of Physiology, Akdeniz University, Antalya, Turkey.
Ozlenen OzkanDepartment of Plastic and Reconstructive Surgery, Akdeniz University, Antalya, Turkey.
Matteo AmorosoDepartment of Plastic Surgery, University of Gothenburg, The Sahlgrenska Academy, Institute of Clinical Sciences, Sahlgrenska University Hospital, Göteborg, Sweden.
Mutay AslanDepartment of Biochemistry, Akdeniz University, Antalya, Turkey.
Ibrahim BassorgunDepartment of Pathology, Akdeniz University, Antalya, Turkey.
Mehmet Can UburDepartment of Plastic and Reconstructive Surgery, Akdeniz University, Antalya, Turkey.
Kerim ÜnalDepartment of Plastic and Reconstructive Surgery, Akdeniz University, Antalya, Turkey.
Filiz OzcanDepartment of Biochemistry, Akdeniz University, Antalya, Turkey.
Omer OzkanDepartment of Plastic and Reconstructive Surgery, Akdeniz University, Antalya, Turkey.
Akdeniz University · TRAkdeniz University Hospital · TRSahlgrenska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIschemic preconditioning (IPC) is defined as raising tolerance to subsequent ischemic stress by exposing tissues to sub-lethal ischemia. Although many candidates have been suggested, recent studies have clearly demonstrated that adenosine-mediated ADORA2B receptor (ADORA2BR) activation is the main mechanism involved in IPC. While the tissue-protective role of this mechanism has been demonstrated in different ischemia/reperfusion (I/R) models, its role in flap surgery-derived I/R damage has not to date been investigated.

objectiveTo investigate the role of adenosine and ADORA2BR activation in IPC-mediated tissue protection in an epigastric flap model.

methodsAnimals were divided into five main groups, all of which were then divided into two subgroups depending on whether or not they were exposed to IPC before the I/R procedure, which consisted of 6 hours of ischemia and 6 days of reperfusion. No drugs were administered in Group 1 (the control group). Animals in Group 2 were pretreated with CD73-inhibitor before IPC application or the ischemic period. Animals in Group 3 were pretreated with adenosine. Animals in Group 4 were pretreated with an ADORA2BR antagonist, and those in Group 5 with an ADORA2BR agonist. After 6 days of reperfusion, tissue survival was evaluated via histological and macroscopic analysis.

resultsIPC application significantly enhanced CD73 expressions and adenosine concentrations (p < 0.01). Flap survivals were increased by IPC in Group 1 (p < 0.05). However, CD73 inhibition blocked this increase (Group 2). In Group 3, adenosine improved flap survival even in the absence of IPC (p < 0.01). While an ADORA2BR antagonist attenuated the tissue-protective effect of IPC (p < 0.01), the ADORA2BR agonist improved flap survival by mimicking IPC in groups 4 and 5.

conclusionThese results provide pharmacological evidence for a contribution of CD73 enzyme-dependent adenosine generation and signaling through ADORA2BR to IPC-mediated tissue protection. They also suggest for the first time that ADORA2BR agonists may be used as a potential preventive therapy against I/R injury in flap surgeries.

Indexed as

AdenosineAnimalsFemaleHumansIschemic PreconditioningRatsRats, WistarReceptor, Adenosine A2BReperfusion InjurySurgical FlapsTissue SurvivalAdenosineADORA2B protein, humanReceptor, Adenosine A2BAdenosineADORA 2Bflap survivalischemiareperfusion

Identifiers

PMID31985456
OpenAlexW3002302730

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.