Evidence map›Paper›PMID 26333362›Full record

ArticleCirculation research2015

miR-206 Mediates YAP-Induced Cardiac Hypertrophy and Survival.

Yanfei Yang, Dominic P Del Re, Noritsugu Nakano, Sebastiano Sciarretta, Peiyong Zhai, Jiyeon Park, Danish Sayed, Akihiro Shirakabe, Shoji Matsushima, Yongkyu Park and 3 more

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In one paragraph

Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

88 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
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28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Yanfei YangFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Dominic P Del ReFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Noritsugu NakanoFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Sebastiano SciarrettaFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Peiyong ZhaiFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Jiyeon ParkFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Danish SayedFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Akihiro ShirakabeFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Shoji MatsushimaFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Yongkyu ParkFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Bin TianFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Maha AbdellatifFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).
Junichi SadoshimaFrom the Cardiovascular Research Institute and the Department of Cell Biology and Molecular Medicine (Y.Y., D.P.D.R., N.N., P.Z., D.S., A.S., S.M., Y.P., M.A., J.S.), and Department of Biochemistry (J.P., B.T.), Rutgers, New Jersey Medical School, Newark; and the Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina and IRCCS Neuromed, Pozzilli (IS), Italy (S.S.).

Funding

Cysteine oxidation in the heartR01HL091469 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI Junichi Sadoshima · 2008 to 2026
$9.4M
The Role of Serine Signaling in Compensatory Cardiac HypertrophyR01HL112330 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI Junichi Sadoshima · 2012 to 2026
$7.5M
The Role of Thioredoxin in the Aging HeartR01AG023039 · NIA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2004 to 2018
$5.8M
Regulation of myocardial growth and death by GSK-3R01HL067724 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2000 to 2018
$5.1M
Regulation of myocardial growth and death by autophagyR01HL102738 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2010 to 2014
$2.5M
The role of NF2 in myocardial ischemia and reperfusion injuryR01HL127339 · NHLBI · RBHS-NEW JERSEY MEDICAL SCHOOL · PI DEL RE, DOMINIC P · 2015 to 2019
$2.0M
Loco/RGS14 Signaling Pathway in LongevityR21AG042021 · NIA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI PARK, YONGKYU · 2013 to 2014
$437k
Alternative mRNA processing in cardiac hypertrophyR21HL098802 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI TIAN, BIN · 2010 to 2011
$429k
The role of RASSF1A in myocardial ischemia/reperfusion injuryR21HL122669 · NHLBI · RBHS-NEW JERSEY MEDICAL SCHOOL · PI DEL RE, DOMINIC P · 2013 to 2013
$159k
NHLBI NIH HHS HL102738NHLBI NIH HHS HL112330NHLBI NIH HHS HL122669NHLBI NIH HHS HL127339NHLBI NIH HHS HL 67724NHLBI NIH HHS HL91469NHLBI NIH HHS R01 HL067724NHLBI NIH HHS R01 HL091469NHLBI NIH HHS R01 HL102738NHLBI NIH HHS R01 HL112330NHLBI NIH HHS R01 HL127339NHLBI NIH HHS R21 HL098802NHLBI NIH HHS R21 HL122669NIA NIH HHS AG23039NIA NIH HHS R01 AG023039NIA NIH HHS R21 AG042021
6 · The paper itself

Abstract

rationaleIn Drosophila, the Hippo signaling pathway negatively regulates organ size by suppressing cell proliferation and survival through the inhibition of Yorkie, a transcriptional cofactor. Yes-associated protein (YAP), the mammalian homolog of Yorkie, promotes cardiomyocyte growth and survival in postnatal hearts. However, the underlying mechanism responsible for the beneficial effect of YAP in cardiomyocytes remains unclear.

objectivesWe investigated whether miR-206, a microRNA known to promote hypertrophy in skeletal muscle, mediates the effect of YAP on promotion of survival and hypertrophy in cardiomyocytes. METHODS AND

resultsMicroarray analysis indicated that YAP increased miR-206 expression in cardiomyocytes. Increased miR-206 expression induced cardiac hypertrophy and inhibited cell death in cultured cardiomyocytes, similar to that of YAP. Downregulation of endogenous miR-206 in cardiomyocytes attenuated YAP-induced cardiac hypertrophy and survival, suggesting that miR-206 plays a critical role in mediating YAP function. Cardiac-specific overexpression of miR-206 in mice induced hypertrophy and protected the heart from ischemia/reperfusion injury, whereas suppression of miR-206 exacerbated ischemia/reperfusion injury and prevented pressure overload-induced cardiac hypertrophy. miR-206 negatively regulates Forkhead box protein P1 expression in cardiomyocytes and overexpression of Forkhead box protein P1 attenuated miR-206-induced cardiac hypertrophy and survival, suggesting that Forkhead box protein P1 is a functional target of miR-206.

conclusionsYAP increases the abundance of miR-206, which in turn plays an essential role in mediating hypertrophy and survival by silencing Forkhead box protein P1 in cardiomyocytes.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAnimals, NewbornApoptosis Regulatory ProteinsCardiomegalyCell Cycle ProteinsCells, CulturedCell SurvivalDisease Models, AnimalForkhead Transcription FactorsGene Expression RegulationMice, TransgenicMicroRNAsMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCell Cycle ProteinsForkhead Transcription FactorsFoxp1 protein, mouseFoxP1 protein, ratMicroRNAsMirn206 microRNA, mousemirn206 microRNA, ratPhosphoproteinsRepressor ProteinsYap1 protein, mouseYap1 protein, ratYAP-Signaling ProteinsapoptosishearthypertrophymicroRNAssignal transduction

Identifiers

PMID26333362
PMCPMC4747867

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