Evidence map›Paper›PMID 31447688›Full record

ArticleFrontiers in physiology2019

Sphingolipid Synthesis Inhibition by Myriocin Administration Enhances Lipid Consumption and Ameliorates Lipid Response to Myocardial Ischemia Reperfusion Injury.

Fabiola Bonezzi, Marco Piccoli, Michele Dei Cas, Rita Paroni, Alessandra Mingione, Michelle M Monasky, Anna Caretti, Chiara Riganti, Riccardo Ghidoni, Carlo Pappone and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Anthonoic Acids A-C, Sulfated andMolecules (Basel, Switzerland) · 2025
    Article
  3. Review
  4. ORMDL in metabolic health and disease.Pharmacology & therapeutics · 2023
    Review
  5. Review
  6. Review
  7. Article
  8. Sphingolipid metabolism and signaling in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  9. Article
  10. Mitochondrial Homeostasis Mediates Lipotoxicity in the Failing Myocardium.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Review
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

12 authors at 3 institutions in 1 country.

Fabiola BonezziStem Cells for Tissue Engineering Laboratory, IRCCS Policlinico San Donato, Milan, Italy.
Marco PiccoliStem Cells for Tissue Engineering Laboratory, IRCCS Policlinico San Donato, Milan, Italy.
Michele Dei CasClinical Biochemistry and Mass Spectrometry Laboratory, Health Sciences Department, University of Milan, Milan, Italy.
Rita ParoniClinical Biochemistry and Mass Spectrometry Laboratory, Health Sciences Department, University of Milan, Milan, Italy.
Alessandra MingioneBiochemistry and Molecular Biology Laboratory, Health Sciences Department, University of Milan, Milan, Italy.
Michelle M MonaskyArrhythmology Department, IRCCS Policlinico San Donato, Milan, Italy.
Anna CarettiBiochemistry and Molecular Biology Laboratory, Health Sciences Department, University of Milan, Milan, Italy.
Chiara RigantiCell Biochemistry Laboratory, Oncology Department, and Interdepartmental Research Center for Molecular Biotechnology, University of Turin, Turin, Italy.
Riccardo GhidoniBiochemistry and Molecular Biology Laboratory, Health Sciences Department, University of Milan, Milan, Italy.
Carlo PapponeArrhythmology Department, IRCCS Policlinico San Donato, Milan, Italy.
Luigi AnastasiaStem Cells for Tissue Engineering Laboratory, IRCCS Policlinico San Donato, Milan, Italy.
Paola SignorelliBiochemistry and Molecular Biology Laboratory, Health Sciences Department, University of Milan, Milan, Italy.
University of Milan · ITIRCCS Policlinico San Donato · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarct requires prompt thrombolytic therapy or primary percutaneous coronary intervention to limit the extent of necrosis, but reperfusion creates additional damage. Along with reperfusion, a maladaptive remodeling phase might occur and it is often associated with inflammation, oxidative stress, as well as a reduced ability to recover metabolism homeostasis. Infarcted individuals can exhibit reduced lipid turnover and their accumulation in cardiomyocytes, which is linked to a deregulation of peroxisome proliferator activated receptors (PPARs), controlling fatty acids metabolism, energy production, and the anti-inflammatory response. We previously demonstrated that Myriocin can be effectively used as post-conditioning therapeutic to limit ischemia/reperfusion-induced inflammation, oxidative stress, and infarct size, in a murine model. In this follow-up study, we demonstrate that Myriocin has a critical regulatory role in cardiac remodeling and energy production, by up-regulating the transcriptional factor EB, PPARs nuclear receptors and genes involved in fatty acids metabolism, such as VLDL receptor, Fatp1, CD36, Fabp3, Cpts, and mitochondrial FA dehydrogenases. The overall effects are represented by an increased β-oxidation, together with an improved electron transport chain and energy production. The potent immunomodulatory and metabolism regulatory effects of Myriocin elicit the molecule as a promising pharmacological tool for post-conditioning therapy of myocardial ischemia/reperfusion injury.

Indexed as

ceramideischemiametabolismmyriocinreperfusionsphingolipids

Identifiers

PMID31447688
PMCPMC6696899
OpenAlexW2961848930

What OpenQuestion holds

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LicenceCC BY
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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.