Evidence map›Paper›PMID 36852954›Full record

ArticleEMBO reports2023

Deregulations of miR-1 and its target Multiplexin promote dilated cardiomyopathy associated with myotonic dystrophy type 1.

Anissa Souidi, Masayuki Nakamori, Monika Zmojdzian, Teresa Jagla, Yoan Renaud, Krzysztof Jagla

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  7. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
    Review
  8. Review
  9. Decoding Nucleotide Repeat Expansion Diseases: Novel Insights fromInternational journal of molecular sciences · 2024
    Review
  10. Article
  11. A case of myotonic dystrophy type 1 with severe dilated cardiomyopathy: an unusual presenting manifestation of the most common muscular dystrophy in adults.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  12. 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

6 authors at 2 institutions in 2 countries.

Anissa SouidiiGReD Genetics Reproduction and Development Institute, Clermont Auvergne University, Clermont-Ferrand, France.
Masayuki NakamoriDepartment of Neurology, Osaka University Graduate School of Medicine, Suita, Japan.
Monika ZmojdzianiGReD Genetics Reproduction and Development Institute, Clermont Auvergne University, Clermont-Ferrand, France.ORCID 0000-0001-6174-2719
Teresa JaglaiGReD Genetics Reproduction and Development Institute, Clermont Auvergne University, Clermont-Ferrand, France.ORCID 0000-0002-9277-6089
Yoan RenaudiGReD Genetics Reproduction and Development Institute, Clermont Auvergne University, Clermont-Ferrand, France.
Krzysztof JaglaiGReD Genetics Reproduction and Development Institute, Clermont Auvergne University, Clermont-Ferrand, France.ORCID 0000-0003-4965-8818
Université Clermont Auvergne · FRThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myotonic dystrophy type 1 (DM1) is the most common muscular dystrophy in adults. It is caused by the excessive expansion of noncoding CTG repeats, which when transcribed affects the functions of RNA-binding factors with adverse effects on alternative splicing, processing, and stability of a large set of muscular and cardiac transcripts. Among these effects, inefficient processing and down-regulation of muscle- and heart-specific miRNA, miR-1, have been reported in DM1 patients, but the impact of reduced miR-1 on DM1 pathogenesis has been unknown. Here, we use Drosophila DM1 models to explore the role of miR-1 in cardiac dysfunction in DM1. We show that miR-1 down-regulation in the heart leads to dilated cardiomyopathy (DCM), a DM1-associated phenotype. We combined in silico screening for miR-1 targets with transcriptional profiling of DM1 cardiac cells to identify miR-1 target genes with potential roles in DCM. We identify Multiplexin (Mp) as a new cardiac miR-1 target involved in DM1. Mp encodes a collagen protein involved in cardiac tube formation in Drosophila. Mp and its human ortholog Col15A1 are both highly enriched in cardiac cells of DCM-developing DM1 flies and in heart samples from DM1 patients with DCM, respectively. When overexpressed in the heart, Mp induces DCM, whereas its attenuation rescues the DCM phenotype of aged DM1 flies. Reduced levels of miR-1 and consecutive up-regulation of its target Mp/Col15A1 might be critical in DM1-associated DCM.

Indexed as

Cardiomyopathy, DilatedMicroRNAsMyotonic DystrophyAdultAgedAnimalsDrosophilaHeartHumansMicroRNAsMIRN1 microRNA, humandilated cardiomyopathyDrosophilamiR-1Multiplexinmyotonic dystrophy type 1

Identifiers

PMID36852954
PMCPMC10074075
OpenAlexW4322616995

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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.