Evidence map›Paper›PMID 32657324›Full record

ArticleEuropean heart journal2020

Targeting muscle-enriched long non-coding RNA H19 reverses pathological cardiac hypertrophy.

Janika Viereck, Anne Bührke, Ariana Foinquinos, Shambhabi Chatterjee, Jan A Kleeberger, Ke Xiao, Heike Janssen-Peters, Sandor Batkai, Deepak Ramanujam, Theresia Kraft and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in European heart journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

94 citing papers in PubMed, 117 citations in OpenAlex.

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  14. Prostaglandin DCells · 2025
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  19. Article
  20. Emerging Roles of Long Non-Coding RNAs in Cardiovascular Diseases.Journal of cellular and molecular medicine · 2025
    Review

34 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 5 institutions in 3 countries.

Janika ViereckInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Anne BührkeInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Ariana FoinquinosInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Shambhabi ChatterjeeInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Jan A KleebergerInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Ke XiaoInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Heike Janssen-PetersInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Sandor BatkaiInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Deepak RamanujamInstitute of Pharmacology and Toxicology, Technische Universität München, Biedersteiner Str. 29, Munich 80802, Germany.
Theresia KraftInstitute for Molecular and Cell Physiology, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Serghei CebotariDepartment of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover, 30625, Germany.
Faikah GuelerDepartment of Nephrology, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover, 30625, Germany.
Andreas M BeyerDepartment of Medicine, Medical College of Wisconsin, Milwaukee, USA.
Jessica SchmitzInstitute for Pathology, Nephropathology Unit, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Jan H BräsenInstitute for Pathology, Nephropathology Unit, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Jan D SchmittoDepartment of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover, 30625, Germany.
Mariann GyöngyösiDepartment of Cardiology, Medical University of Vienna, Austria.
Alexandra LöserDepartment of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Marc N HirtDepartment of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Thomas EschenhagenDepartment of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Stefan EngelhardtInstitute of Pharmacology and Toxicology, Technische Universität München, Biedersteiner Str. 29, Munich 80802, Germany.
Christian BärInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Thomas ThumInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany.
Medizinische Hochschule Hannover · DEUniversität Hamburg · DEGerman Centre for Cardiovascular Research · DEMedical College of Wisconsin · USMedical University of Vienna · AT

Funding

Pivotal Role of Mitochondrial Telomerase in Regulation of Vascular Tone and Redox HomeostasisR01HL133029 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI BEYER, ANDREAS M · 2017 to 2021
$2.2M
NHLBI NIH HHS R01 HL133029
6 · The paper itself

Abstract

aimsPathological cardiac remodelling and subsequent heart failure represents an unmet clinical need. Long non-coding RNAs (lncRNAs) are emerging as crucial molecular orchestrators of disease processes, including that of heart diseases. Here, we report on the powerful therapeutic potential of the conserved lncRNA H19 in the treatment of pathological cardiac hypertrophy. METHOD AND

resultsPressure overload-induced left ventricular cardiac remodelling revealed an up-regulation of H19 in the early phase but strong sustained repression upon reaching the decompensated phase of heart failure. The translational potential of H19 is highlighted by its repression in a large animal (pig) model of left ventricular hypertrophy, in diseased human heart samples, in human stem cell-derived cardiomyocytes and in human engineered heart tissue in response to afterload enhancement. Pressure overload-induced cardiac hypertrophy in H19 knock-out mice was aggravated compared to wild-type mice. In contrast, vector-based, cardiomyocyte-directed gene therapy using murine and human H19 strongly attenuated heart failure even when cardiac hypertrophy was already established. Mechanistically, using microarray, gene set enrichment analyses and Chromatin ImmunoPrecipitation DNA-Sequencing, we identified a link between H19 and pro-hypertrophic nuclear factor of activated T cells (NFAT) signalling. H19 physically interacts with the polycomb repressive complex 2 to suppress H3K27 tri-methylation of the anti-hypertrophic Tescalcin locus which in turn leads to reduced NFAT expression and activity.

conclusionH19 is highly conserved and down-regulated in failing hearts from mice, pigs and humans. H19 gene therapy prevents and reverses experimental pressure-overload-induced heart failure. H19 acts as an anti-hypertrophic lncRNA and represents a promising therapeutic target to combat pathological cardiac remodelling.

Indexed as

Heart DiseasesHeart FailureRNA, Long NoncodingAnimalsCardiomegalyDisease Models, AnimalHumansHypertrophy, Left VentricularMiceMice, KnockoutMyocytes, CardiacSwineH19 long non-coding RNARNA, Long NoncodingCardiovascular diseaseGene therapyHypertrophyLong non-coding RNATranslational research

Identifiers

PMID32657324
PMCPMC8482849
OpenAlexW3042719469

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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.