Evidence map›Paper›PMID 25521429›Full record

ArticleBritish journal of pharmacology2015

Structural apelin analogues: mitochondrial ROS inhibition and cardiometabolic protection in myocardial ischaemia reperfusion injury.

Oleg Pisarenko, Valentin Shulzhenko, Irina Studneva, Yulia Pelogeykina, Alexander Timoshin, Rodica Anesia, Philippe Valet, Angelo Parini, Oksana Kunduzova

Open access · hybridAbstract read
In one paragraph

Article in British journal of pharmacology, 2015. 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
4.9field-weighted citation impact, top 5% 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, 63 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
  6. Article
  7. Review
  8. A Review of the Roles of Apelin and ELABELA Peptide Ligands in Cardiovascular Disease, Including Heart Failure and Hypertension.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Review
  9. Article
  10. Article
  11. Induced dysregulation of ACE2 by SARS-CoV-2 plays a key role in COVID-19 severity.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  12. Article
  13. Article
  14. Apelin/APJ-Manipulated CaMKK/AMPK/GSK3Oxidative medicine and cellular longevity · 2021
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

9 authors at 3 institutions in 2 countries.

Oleg PisarenkoRussian Cardiology Research-and-Production Complex, Moscow, Russia.
Valentin ShulzhenkoRussian Cardiology Research-and-Production Complex, Moscow, Russia.
Irina StudnevaRussian Cardiology Research-and-Production Complex, Moscow, Russia.
Yulia PelogeykinaRussian Cardiology Research-and-Production Complex, Moscow, Russia.
Alexander TimoshinRussian Cardiology Research-and-Production Complex, Moscow, Russia.
Rodica AnesiaNational Institute of Health and Medical Research (INSERM) U1048, Toulouse, France.
Philippe ValetNational Institute of Health and Medical Research (INSERM) U1048, Toulouse, France.
Angelo PariniNational Institute of Health and Medical Research (INSERM) U1048, Toulouse, France.
Oksana KunduzovaNational Institute of Health and Medical Research (INSERM) U1048, Toulouse, France.
Institute of Experimental Cardiology · RUUniversité Toulouse III - Paul Sabatier · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeMitochondria-derived oxidative stress is believed to be crucially involved in cardiac ischaemia reperfusion (I/R) injury, although currently no therapies exist that specifically target mitochondrial reactive oxygen species (ROS) production. The present study was designed to evaluate the potential effects of the structural analogues of apelin-12, an adipocyte-derived peptide, on mitochondrial ROS generation, cardiomyocyte apoptosis, and metabolic and functional recovery to myocardial I/R injury. EXPERIMENTAL APPROACH: In cultured H9C2 cardiomyoblasts and adult cardiomyocytes, oxidative stress was induced by hypoxia reoxygenation. Isolated rat hearts were subjected to 35 min of global ischaemia and 30 min of reperfusion. Apelin-12, apelin-13 and structural apelin-12 analogues, AI and AII, were infused during 5 min prior to ischaemia. KEY

resultsIn cardiac cells, mitochondrial ROS production was inhibited by the structural analogues of apelin, AI and AII, in comparison with the natural peptides, apelin-12 and apelin-13. Treatment of cardiomyocytes with AI and AII decreased cell apoptosis concentration-dependently. In a rat model of I/R injury, pre-ischaemic infusion of AI and AII markedly reduced ROS formation in the myocardial effluent and attenuated cell membrane damage. Prevention of oxidative damage by AI and AII was associated with the improvement of functional and metabolic recovery after I/R in the heart. CONCLUSIONS AND IMPLICATIONS: These data provide the evidence for the potential of the structural apelin analogues in selective reduction of mitochondrial ROS generation and myocardial apoptosis and form the basis for a promising therapeutic strategy in the treatment of oxidative stress-related heart disease.

Indexed as

AnimalsApoptosisCell MembraneDose-Response Relationship, DrugIntercellular Signaling Peptides and ProteinsMaleMitochondriaMyocardial Reperfusion InjuryMyocytes, CardiacOxidative StressRatsRats, WistarReactive Oxygen Speciesapelin-12 peptideapelin-13 peptideIntercellular Signaling Peptides and ProteinsReactive Oxygen Species

Identifiers

PMID25521429
PMCPMC4459014
OpenAlexW1487226011

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.