Evidence map›Paper›PMID 36233322›Full record

ArticleInternational journal of molecular sciences2022

Desmin Knock-Out Cardiomyopathy: A Heart on the Verge of Metabolic Crisis.

Barbara Elsnicova, Daniela Hornikova, Veronika Tibenska, David Kolar, Tereza Tlapakova, Benjamin Schmid, Markus Mallek, Britta Eggers, Ursula Schlötzer-Schrehardt, Viktoriya Peeva and 13 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Article
  8. Research Progress in Skin Aging, Metabolism, and Related Products.International journal of molecular sciences · 2023
    Review
  9. Nucleus Mechanosensing in Cardiomyocytes.International journal of molecular sciences · 2023
    Review
  10. Article
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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

23 authors at 8 institutions in 3 countries.

Barbara ElsnicovaDepartment of Physiology, Faculty of Science, Charles University, 128 00 Prague, Czech Republic.
Daniela HornikovaDepartment of Physiology, Faculty of Science, Charles University, 128 00 Prague, Czech Republic.
Veronika TibenskaDepartment of Physiology, Faculty of Science, Charles University, 128 00 Prague, Czech Republic.
David KolarDepartment of Physiology, Faculty of Science, Charles University, 128 00 Prague, Czech Republic.
Tereza TlapakovaDepartment of Cell Biology, Faculty of Science, Charles University, 128 00 Prague, Czech Republic.ORCID 0000-0001-8841-1573
Benjamin SchmidOptical Imaging Center Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91058 Erlangen, Germany.ORCID 0000-0002-9327-2296
Markus MallekMVZ Dr. Eberhard & Partner Dortmund, 44137 Dortmund, Germany.
Britta EggersMedizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801 Bochum, Germany.
Ursula Schlötzer-SchrehardtDepartment of Ophthalmology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany.
Viktoriya PeevaDivision of Neurochemistry, Institute of Experimental Epileptology and Cognition Research, University of Bonn, 53127 Bonn, Germany.ORCID 0000-0001-8007-017X
Carolin BerwangerInstitute of Aerospace Medicine, German Aerospace Center (DLR), Linder Höhe, 51147 Cologne, Germany.
Bettina EberhardMVZ Dr. Eberhard & Partner Dortmund, 44137 Dortmund, Germany.
Hacer DurmuşDepartment of Neurology, Istanbul Faculty of Medicine, Istanbul University, 34093 Istanbul, Turkey.
Dorothea SchultheisInstitute of Neuropathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany.
Christian HoltzhausenInstitute of Neuropathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany.
Karin SchorkMedizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801 Bochum, Germany.ORCID 0000-0003-3756-4347
Katrin MarcusMedizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801 Bochum, Germany.ORCID 0000-0002-3313-8845
Jens JordanInstitute of Aerospace Medicine, German Aerospace Center (DLR), Linder Höhe, 51147 Cologne, Germany.
Thomas LückeUniversity Hospital of Pediatrics and Adolescent Medicine, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany.
Peter F M van der VenDepartment of Molecular Cell Biology, Institute for Cell Biology, University of Bonn, 53121 Bonn, Germany.ORCID 0000-0002-9750-8913
Rolf SchröderInstitute of Neuropathology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany.
Christoph S ClemenInstitute of Aerospace Medicine, German Aerospace Center (DLR), Linder Höhe, 51147 Cologne, Germany.ORCID 0000-0002-1291-4219
Jitka M ZurmanovaDepartment of Physiology, Faculty of Science, Charles University, 128 00 Prague, Czech Republic.
Charles University · CZFriedrich-Alexander-Universität Erlangen-Nürnberg · DERuhr University Bochum · DEUniversity of Bonn · DEUniversity of Cologne · DEDeutsches Zentrum für Luft- und Raumfahrt e. V. (DLR) · DEIstanbul University · TRSt. Josef-Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Desmin mutations cause familial and sporadic cardiomyopathies. In addition to perturbing the contractile apparatus, both desmin deficiency and mutated desmin negatively impact mitochondria. Impaired myocardial metabolism secondary to mitochondrial defects could conceivably exacerbate cardiac contractile dysfunction. We performed metabolic myocardial phenotyping in left ventricular cardiac muscle tissue in desmin knock-out mice. Our analyses revealed decreased mitochondrial number, ultrastructural mitochondrial defects, and impaired mitochondria-related metabolic pathways including fatty acid transport, activation, and catabolism. Glucose transporter 1 and hexokinase-1 expression and hexokinase activity were increased. While mitochondrial creatine kinase expression was reduced, fetal creatine kinase expression was increased. Proteomic analysis revealed reduced expression of proteins involved in electron transport mainly of complexes I and II, oxidative phosphorylation, citrate cycle, beta-oxidation including auxiliary pathways, amino acid catabolism, and redox reactions and oxidative stress. Thus, desmin deficiency elicits a secondary cardiac mitochondriopathy with severely impaired oxidative phosphorylation and fatty and amino acid metabolism. Increased glucose utilization and fetal creatine kinase upregulation likely portray attempts to maintain myocardial energy supply. It may be prudent to avoid medications worsening mitochondrial function and other metabolic stressors. Therapeutic interventions for mitochondriopathies might also improve the metabolic condition in desmin deficient hearts.

Indexed as

CardiomyopathiesDesminHexokinaseAmino AcidsAnimalsCitratesCreatine Kinase, Mitochondrial FormFatty AcidsGlucoseGlucose Transporter Type 1MiceMice, KnockoutMyocardiumOxidative PhosphorylationProteomicsAmino AcidsCitratesCreatine Kinase, Mitochondrial FormDesminFatty AcidsGlucoseGlucose Transporter Type 1Hexokinaseamino acidcardiomyopathycreatine kinasedesmindesmin knock-out metabolismdesminopathyfatty acidglucosemitochondriamitochondriopathy

Identifiers

PMID36233322
PMCPMC9570457
OpenAlexW4303981427

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.