Evidence map›Paper›PMID 30219874›Full record

ArticleEuropean heart journal2018

Myeloperoxidase is a potential molecular imaging and therapeutic target for the identification and stabilization of high-risk atherosclerotic plaque.

Imran Rashid, Ghassan J Maghzal, Yung-Chih Chen, David Cheng, Jihan Talib, Darren Newington, Minqin Ren, Saumitra K Vajandar, Amy Searle, Ana Maluenda and 8 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in European heart journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Neutrophil extracellular traps: a catalyst for atherosclerosis.Molecular and cellular biochemistry · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 6 institutions in 4 countries.

Imran RashidVascular Biology Division, Victor Chang Cardiac Research Institute, Lowy Packer Building, 405 Liverpool Street, Darlinghurst NSW, Australia.
Ghassan J MaghzalVascular Biology Division, Victor Chang Cardiac Research Institute, Lowy Packer Building, 405 Liverpool Street, Darlinghurst NSW, Australia.
Yung-Chih ChenAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, 75 Commercial Road Melbourne, VIC, Australia.
David ChengVascular Biology Division, Victor Chang Cardiac Research Institute, Lowy Packer Building, 405 Liverpool Street, Darlinghurst NSW, Australia.
Jihan TalibVascular Biology Division, Victor Chang Cardiac Research Institute, Lowy Packer Building, 405 Liverpool Street, Darlinghurst NSW, Australia.
Darren NewingtonVascular Biology Division, Victor Chang Cardiac Research Institute, Lowy Packer Building, 405 Liverpool Street, Darlinghurst NSW, Australia.
Minqin RenDepartment of Physics, Centre for Ion Beam Applications, National University of Singapore, 2 Science Drive 3, Singapore, Singapore.
Saumitra K VajandarDepartment of Physics, Centre for Ion Beam Applications, National University of Singapore, 2 Science Drive 3, Singapore, Singapore.
Amy SearleAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, 75 Commercial Road Melbourne, VIC, Australia.
Ana MaluendaAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, 75 Commercial Road Melbourne, VIC, Australia.
Eva-Lotte LindstedtBioscience Heart Failure, Cardiovascular, Renal and Metabolism, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.
Andrew JabbourVascular Biology Division, Victor Chang Cardiac Research Institute, Lowy Packer Building, 405 Liverpool Street, Darlinghurst NSW, Australia.
Antony J KettleCentre for Free Radical Research, University of Otago Christchurch, Christchurch, New Zealand.
Andre BongersBiological Resources Imaging Laboratory, University of New South Wales, High Street, Sydney NSW, Australia.
Carl PowerBiological Resources Imaging Laboratory, University of New South Wales, High Street, Sydney NSW, Australia.
Erik MichaëlssonBioscience Heart Failure, Cardiovascular, Renal and Metabolism, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.
Karlheinz PeterAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, 75 Commercial Road Melbourne, VIC, Australia.
Roland StockerVascular Biology Division, Victor Chang Cardiac Research Institute, Lowy Packer Building, 405 Liverpool Street, Darlinghurst NSW, Australia.
Victor Chang Cardiac Research Institute · AUBaker Heart and Diabetes Institute · AUAstraZeneca (Sweden) · SENational University of Singapore · SGUNSW Sydney · AUUniversity of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aims: As the inflammatory enzyme myeloperoxidase (MPO) is abundant in ruptured human atherosclerotic plaques, we aimed to investigate the role of MPO as a potential diagnostic and therapeutic target for high-risk plaque. Methods and results: We employed the tandem stenosis model of atherosclerotic plaque instability in apolipoprotein E gene knockout (Apoe-/-) mice. To test the role of MPO, we used Mpo-/-Apoe-/- mice and the 2-thioxanthine MPO inhibitor AZM198. In vivo MPO activity was assessed by liquid chromatography-tandem mass spectrometry detection of 2-chloroethidium generation from hydroethidine and by bis-5HT-DTPA-Gd (MPO-Gd) molecular magnetic resonance imaging (MRI), while plaque phenotype was verified histologically. Myeloperoxidase activity was two-fold greater in plaque with unstable compared with stable phenotype. Genetic deletion of MPO significantly increased fibrous cap thickness, and decreased plaque fibrin and haemosiderin content in plaque with unstable phenotype. AZM198 inhibited MPO activity and it also increased fibrous cap thickness and decreased fibrin and haemosiderin in plaque with unstable phenotype, without affecting lesion monocytes and red blood cell markers or circulating leukocytes and lipids. MPO-Gd MRI demonstrated sustained enhancement of plaque with unstable phenotype on T1-weighted imaging that was two-fold greater than stable plaque and was significantly attenuated by both AZM198 treatment and deletion of the Mpo gene. Conclusion: Our data implicate MPO in atherosclerotic plaque instability and suggest that non-invasive imaging and pharmacological inhibition of plaque MPO activity hold promise for clinical translation in the management of high-risk coronary artery disease.

Indexed as

Molecular ImagingAnimalsAtherosclerosisDisease Models, AnimalFibrinHemosiderinMagnetic Resonance ImagingMass SpectrometryMice, KnockoutPeroxidasePlaque, AtheroscleroticThioxanthenes2-thioxantheneFibrinHemosiderinPeroxidaseThioxanthenes

Identifiers

PMID30219874
OpenAlexW2884420067

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.