Evidence map›Paper›PMID 37009793›Full record

ArticleExperimental & molecular medicine2023

Altered acylcarnitine metabolism and inflexible mitochondrial fuel utilization characterize the loss of neonatal myocardial regeneration capacity.

E Kankuri, P Finckenberg, J Leinonen, M Tarkia, S Björk, J Purhonen, J Kallijärvi, M Kankainen, R Soliymani, M Lalowski and 1 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Membrane Stress and Ferroptosis: Lipid Dynamics in Cancer.International journal of molecular sciences · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Progress of Mitochondrial Function Regulation in Cardiac Regeneration.Journal of cardiovascular translational research · 2024
    Review
  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

11 authors at 1 institution in 2 countries.

E KankuriDepartment of Pharmacology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.ORCID 0000-0002-2193-8773
P FinckenbergDepartment of Pharmacology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
J LeinonenDepartment of Pharmacology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.ORCID 0000-0001-8127-078X
M TarkiaDepartment of Pharmacology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
S BjörkDepartment of Pharmacology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
J PurhonenFolkhälsan Research Center, Helsinki, Finland.
J KallijärviFolkhälsan Research Center, Helsinki, Finland.
M KankainenMedical and Clinical Genetics, Faculty of Medicine, University of Helsinki, Helsinki University Hospital, Helsinki, Finland.
R SoliymaniHelsinki Institute of Life Science (HiLIFE), Meilahti Clinical Proteomics Core Facility, Department of Biochemistry and Developmental Biology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
M LalowskiHelsinki Institute of Life Science (HiLIFE), Meilahti Clinical Proteomics Core Facility, Department of Biochemistry and Developmental Biology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
E MervaalaDepartment of Pharmacology, Faculty of Medicine, University of Helsinki, Helsinki, Finland. eero.mervaala@helsinki.fi.
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial regeneration capacity declines during the first week after birth, and this decline is linked to adaptation to oxidative metabolism. Utilizing this regenerative window, we characterized the metabolic changes in myocardial injury in 1-day-old regeneration-competent and 7-day-old regeneration-compromised mice. The mice were either sham-operated or received left anterior descending coronary artery ligation to induce myocardial infarction (MI) and acute ischemic heart failure. Myocardial samples were collected 21 days after operations for metabolomic, transcriptomic and proteomic analyses. Phenotypic characterizations were carried out using echocardiography, histology and mitochondrial structural and functional assessments. In both groups, MI induced an early decline in cardiac function that persisted in the regeneration-compromised mice over time. By integrating the findings from metabolomic, transcriptomic and proteomic examinations, we linked regeneration failure to the accumulation of long-chain acylcarnitines and insufficient metabolic capacity for fatty acid beta-oxidation. Decreased expression of the redox-sensitive mitochondrial Slc25a20 carnitine-acylcarnitine translocase together with a decreased reduced:oxidized glutathione ratio in the myocardium in the regeneration-compromised mice pointed to a defect in the redox-sensitive acylcarnitine transport to the mitochondrial matrix. Rather than a forced shift from the preferred adult myocardial oxidative fuel source, our results suggest the facilitation of mitochondrial fatty acid transport and improvement of the beta-oxidation pathway as a means to overcome the metabolic barrier for repair and regeneration in adult mammals after MI and heart failure.

Indexed as

Heart FailureMyocardial InfarctionAnimalsCarnitineFatty AcidsMammalsMiceMyocardiumProteomicsacylcarnitineCarnitineFatty Acids

Identifiers

PMID37009793
PMCPMC10167339
OpenAlexW4362507486

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.