Evidence map›Paper›PMID 36172949›Full record

ArticleJournal of the American Heart Association2022

Disruption of Sarcoplasmic Reticulum-Mitochondrial Contacts Underlies Contractile Dysfunction in Experimental and Human Atrial Fibrillation: A Key Role of Mitofusin 2.

Jin Li, Xi Qi, Kennedy S Ramos, Eva Lanters, Jaap Keijer, Natasja de Groot, Bianca Brundel, Deli Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Mitochondrial Adaptation to Mechanical Stress in Cardiac Ageing and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Dysfunctional cardiomyocyte signalling and heart disease.Current opinion in cell biology · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

8 authors at 5 institutions in 2 countries.

Jin LiDepartment of Physiology Amsterdam UMC location Vrije Universiteit Amsterdam Amsterdam The Netherlands.ORCID 0000-0002-5743-696X
Xi QiHuman and Animal Physiology Wageningen University Wageningen The Netherlands.
Kennedy S RamosDepartment of Physiology Amsterdam UMC location Vrije Universiteit Amsterdam Amsterdam The Netherlands.ORCID 0000-0002-0283-3765
Eva LantersDepartment of Cardiology Erasmus Medical Center Rotterdam The Netherlands.
Jaap KeijerHuman and Animal Physiology Wageningen University Wageningen The Netherlands.ORCID 0000-0002-9720-7491
Natasja de GrootDepartment of Cardiology Erasmus Medical Center Rotterdam The Netherlands.ORCID 0000-0002-0259-6691
Bianca BrundelDepartment of Physiology Amsterdam UMC location Vrije Universiteit Amsterdam Amsterdam The Netherlands.ORCID 0000-0002-4768-234X
Deli ZhangDepartment of Physiology Amsterdam UMC location Vrije Universiteit Amsterdam Amsterdam The Netherlands.ORCID 0000-0002-8891-9665
Amsterdam Neuroscience · NLErasmus MC · NLWageningen University & Research · NLGraduate School Experimental Plant Sciences · NLUniversity of Michigan · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background Atrial fibrillation (AF) is the most common and progressive tachyarrhythmia. Diabetes is a common risk factor for AF. Recent research findings revealed that microtubule network disruption underlies AF. The microtubule network mediates the contact between sarcoplasmic reticulum and mitochondria, 2 essential organelles for normal cardiomyocyte function. Therefore, disruption of the microtubule network may impair sarcoplasmic reticulum and mitochondrial contacts (SRMCs) and subsequently cardiomyocyte function. The current study aims to determine whether microtubule-mediated SRMCs disruption underlies diabetes-associated AF. Methods and Results Tachypacing (mimicking AF) and high glucose (mimicking diabetes) significantly impaired contractile function in HL-1 cardiomyocytes (loss of calcium transient) and

Indexed as

Atrial FibrillationGTP PhosphohydrolasesMitochondrial ProteinsSarcoplasmic ReticulumAnimalsCalciumDrosophilaDrosophila ProteinsGlucoseHumansMembrane ProteinsMitochondriaMyocytes, CardiacCalciumDrosophila ProteinsGlucoseGTP PhosphohydrolasesMarf protein, DrosophilaMembrane ProteinsMFN2 protein, humanMitochondrial Proteinsatrial fibrillationdiabetesDrosophilamicrotubulesmitosusin 2sarcoplasmic reticulum‐mitochondrial contacts

Identifiers

PMID36172949
PMCPMC9673721
OpenAlexW4297965477

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.