Evidence map›Paper›PMID 24481529›Full record

ArticleCell research2014

Multifaceted roles of miR-1s in repressing the fetal gene program in the heart.

Yusheng Wei, Siwu Peng, Meng Wu, Ravi Sachidanandam, Zhidong Tu, Shihong Zhang, Christine Falce, Eric A Sobie, Djamel Lebeche, Yong Zhao

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
2.2field-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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Deceiving the gatekeepers: virus modulation of gap junctions.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. MicroRNAs in chronic pediatric diseases (Review).Experimental and therapeutic medicine · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Sarcomere maturation: function acquisition, molecular mechanism, and interplay with other organelles.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Review
  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

10 authors at 2 institutions in 1 country.

Yusheng Wei1] Mindich Child Health and Development Institute, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1040, New York, NY 10029, USA [2] Current address: College of Life Sciences, Peking University, Beijing 100871, China.
Siwu PengMindich Child Health and Development Institute, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1040, New York, NY 10029, USA.
Meng WuMindich Child Health and Development Institute, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1040, New York, NY 10029, USA.
Ravi SachidanandamInstitute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Zhidong TuInstitute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Shihong ZhangCardiovascular Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Christine FalcePharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Eric A SobiePharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Djamel LebecheCardiovascular Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Yong ZhaoMindich Child Health and Development Institute, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1040, New York, NY 10029, USA.
Icahn School of Medicine at Mount Sinai · USChild Health and Development Institute · US

Funding

Genetic Analysis of microRNAs Function in Diabetic CardiomyopathyR01HL097357 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEBECHE, DJAMEL · 2010 to 2014
$2.1M
MIR-1-2 FUNCTION IN CARDIAC CONDUCTION SYSTEM DEVELOPMENT AND MAINTENANCER01HL107376 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ZHAO, YONG · 2011 to 2015
$2.0M
UNDERSTANDING THE ROLES OF MIR-1S IN REGULATING HEART DEVELOPMENTK02HL103597 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ZHAO, YONG · 2011 to 2015
$512k
NHLBI NIH HHS 1K02HL103597NHLBI NIH HHS 1R01HL107376NHLBI NIH HHS K02 HL103597NHLBI NIH HHS R01 HL097357NHLBI NIH HHS R01HL097357NHLBI NIH HHS R01 HL107376
6 · The paper itself

Abstract

miRNAs are an important class of regulators that play roles in cellular homeostasis and disease. Muscle-specific miRNAs, miR-1-1 and miR-1-2, have been found to play important roles in regulating cell proliferation and cardiac function. Redundancy between miR-1-1 and miR-1-2 has previously impeded a full understanding of their roles in vivo. To determine how miR-1s regulate cardiac function in vivo, we generated mice lacking miR-1-1 and miR-1-2 without affecting nearby genes. miR-1 double knockout (miR-1 dKO) mice were viable and not significantly different from wild-type controls at postnatal day 2.5. Thereafter, all miR-1 dKO mice developed dilated cardiomyopathy (DCM) and died before P17. Massively parallel sequencing showed that a large portion of upregulated genes after deletion of miR-1s is associated with the cardiac fetal gene program including cell proliferation, glycolysis, glycogenesis, and fetal sarcomere-associated genes. Consistent with gene profiling, glycogen content and glycolytic rates were significantly increased in miR-1 dKO mice. Estrogen-related Receptor β (Errβ) was identified as a direct target of miR-1, which can regulate glycolysis, glycogenesis, and the expression of sarcomeric proteins. Cardiac-specific overexpression of Errβ led to glycogen storage, cardiac dilation, and sudden cardiac death around 3-4 weeks of age. We conclude that miR-1 and its primary target Errβ act together to regulate the transition from prenatal to neonatal stages by repressing the cardiac fetal gene program. Loss of this regulation leads to a neonatal DCM.

Indexed as

3' Untranslated RegionsAnimalsBase SequenceCardiomyopathy, DilatedCell ProliferationCells, CulturedEnergy MetabolismGlycogenGlycolysisMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroRNAsMyocardiumMyocytes, Cardiac3' Untranslated Regionsestrogen receptor-related receptor betaGlycogenMicroRNAsReceptors, Estrogen

Identifiers

PMID24481529
PMCPMC3945888
OpenAlexW2000298831

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.