Evidence map›Paper›PMID 31911566›Full record

ArticleAnatolian journal of cardiology2020

Ischemic postconditioning reduced myocardial ischemia-reperfusion injury: The roles of melatonin and uncoupling protein 3.

Gülnur Aslan, Hüseyin Fatih Gül, Ahmet Tektemur, Engin Sahna

Open access · diamondAbstract read
In one paragraph

Article in Anatolian journal of cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

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  10. Irisin: A Promising Target for Ischemia-Reperfusion Injury Therapy.Oxidative medicine and cellular longevity · 2021
    Review
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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 1 institution in 1 country.

Gülnur AslanDepartment of Pharmacology, Faculty of Medicine, Firat University, Elazig, TURKEY.
Hüseyin Fatih GülDepartment of Biochemistry, Faculty of Medicine, Firat University, Elazig, TURKEY.
Ahmet TektemurDepartment of Medical Biology, Faculty of Medicine, Firat University, Elazig, TURKEY.
Engin SahnaDepartment of Pharmacology, Faculty of Medicine, Firat University, Elazig, TURKEY.
Fırat University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveProtective effects of ischemic postconditioning (PostC) decrease/disappear with age and chronic heart diseases. Similarly, low serum melatonin levels have been reported in the same risk groups. The aims of this study were to investigate the effects of melatonin on the protection of PostC in ischemia-reperfusion (I/R)-induced infarct size and roles of uncoupling protein (UCP) 3, irisin, and nuclear factor kappa B (NFkB) levels.

methodsRats were pinealectomized (Px) or sham operated (non-Px) 2 months before the I/R studies. The left main coronary artery was occluded for 30 min followed by 120 min reperfusion. PostC was induced with three cycles of R/I (10 s each) after ischemia.

resultsThe infarct size was found to be significantly higher in Px rats (54.68±1.5%) than in the control group (35.1±2.5%). PostC and melatonin administrations to non-Px rats significantly reduced the infarct size. On the other hand, PostC did not create a significant effect in Px rats, but protection was provided when PostC was co-administrated with melatonin. While significant decreases were detected in the UCP3 levels, irisin and NFkB levels increased with I/R and Px. Treatment with PostC and melatonin in non-Px groups and their co-administration in Px groups were found to return all the genes close to normal levels.

conclusionThe physiological and pharmacological concentrations of melatonin may play a role in the protection of PostC. In cases when physiological melatonin is reduced, such as aging and heart diseases, this protection may decrease, and this effect may be restored by melatonin replacement. PostC and melatonin may regulate energy metabolism and inflammatory mediators and protect mitochondria by affecting the UCP3, irisin, and NFkB levels.

Indexed as

Ischemic PostconditioningAnimalsDisease Models, AnimalMaleMelatoninMyocardial Reperfusion InjuryRatsRats, Sprague-DawleyUncoupling Protein 3MelatoninUncoupling Protein 3

Identifiers

PMID31911566
PMCPMC7141427
OpenAlexW2972112169

What OpenQuestion holds

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LicenceCC BY-NC-SA
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Registered trials

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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.