Evidence map›Paper›PMID 32341350›Full record

ArticleNature communications2020

Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.

D Julia Trembinski, Diewertje I Bink, Kosta Theodorou, Janina Sommer, Ariane Fischer, Anke van Bergen, Chao-Chung Kuo, Ivan G Costa, Christoph Schürmann, Matthias S Leisegang and 22 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Long Non-coding RNA Based Therapy for Cardiovascular Disease.Journal of cardiovascular translational research · 2025
    Review
  6. Article
  7. Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025
    Review
  8. Review
  9. Article
  10. The relevance of RNA-DNA interactions as regulators of physiological functions.Pflugers Archiv : European journal of physiology · 2025
    Review
  11. Time's imprint on the left atrium: aging and atrial myopathy.The journal of cardiovascular aging · 2025
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Endothelial derived, secreted long non-coding RNAsMolecular therapy. Nucleic acids · 2024
    Article

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

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

32 authors at 12 institutions in 3 countries.

D Julia TrembinskiInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Diewertje I BinkDepartment of Physiology, VU University Medical Center, Amsterdam, the Netherlands.
Kosta TheodorouInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Janina SommerInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Ariane FischerInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Anke van BergenDepartment of Physiology, VU University Medical Center, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-1843-5657
Chao-Chung KuoInstitute for Computational Genomics, Joint Research Center for Computational Biomedicine, RWTH Aachen University, Aachen, Germany.ORCID http://orcid.org/0000-0001-8879-4754
Ivan G CostaInstitute for Computational Genomics, Joint Research Center for Computational Biomedicine, RWTH Aachen University, Aachen, Germany.ORCID http://orcid.org/0000-0003-2890-8697
Christoph SchürmannInstitute for Cardiovascular Physiology, Medical Faculty, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Matthias S LeisegangGerman Center for Cardiovascular Research (DZHK), Berlin, Germany.ORCID http://orcid.org/0000-0002-6084-6484
Ralf P BrandesGerman Center for Cardiovascular Research (DZHK), Berlin, Germany.ORCID http://orcid.org/0000-0002-8035-0048
Tijna AlekseevaGeorg Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Boris BrillGeorg Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Astrid WietelmannMax-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Christopher N JohnsonDivision of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, USA.
Alexander Spring-ConnellDepartment of Chemistry, Georgia State University, Atlanta, USA.
Manuel KaulichInstitute of Biochemistry II, Goethe University, Frankfurt am Main, Germany.ORCID http://orcid.org/0000-0002-9528-8822
Stanislas WerfelGerman Center for Cardiovascular Research (DZHK), Berlin, Germany.
Stefan EngelhardtGerman Center for Cardiovascular Research (DZHK), Berlin, Germany.ORCID http://orcid.org/0000-0001-5378-8661
Marc N HirtGerman Center for Cardiovascular Research (DZHK), Berlin, Germany.
Kaja YorganGerman Center for Cardiovascular Research (DZHK), Berlin, Germany.
Thomas EschenhagenGerman Center for Cardiovascular Research (DZHK), Berlin, Germany.ORCID http://orcid.org/0000-0003-1750-1170
Luisa KirchhofInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Patrick HofmannInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Nicolas JaéInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Ilka WittigGerman Center for Cardiovascular Research (DZHK), Berlin, Germany.
Nazha HamdaniDepartment of Physiology, VU University Medical Center, Amsterdam, the Netherlands.
Corinne BischofInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Jaya KrishnanInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Riekelt H HoutkooperLaboratory Genetic Metabolic Diseases, Academic Medical Center, Amsterdam, the Netherlands.
Stefanie DimmelerInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.
Reinier A BoonInstitute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany. Boon@med.uni-frankfurt.de.ORCID http://orcid.org/0000-0001-7944-9748
Goethe University Frankfurt · DEUniversität Hamburg · DEAmsterdam UMC Location Vrije Universiteit Amsterdam · NLGeorg Speyer Haus · DERWTH Aachen University · DEAmsterdam UMC Location University of Amsterdam · NLGeorgia State University · USGerman Centre for Cardiovascular Research · DEMax Planck Institute for Heart and Lung Research · DERuhr University Bochum · DETUM Klinikum · DEVanderbilt University Medical Center · US

Funding

Console upgrades for biological NMR spectrometersS10RR025677 · NCRR · VANDERBILT UNIVERSITY · PI SANDERS, CHARLES R · 2009 to 2009
$460k
Medical Research Council MC_UP_1102/4NCRR NIH HHS S10 RR025677
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) contribute to cardiac (patho)physiology. Aging is the major risk factor for cardiovascular disease with cardiomyocyte apoptosis as one underlying cause. Here, we report the identification of the aging-regulated lncRNA Sarrah (ENSMUST00000140003) that is anti-apoptotic in cardiomyocytes. Importantly, loss of SARRAH (OXCT1-AS1) in human engineered heart tissue results in impaired contractile force development. SARRAH directly binds to the promoters of genes downregulated after SARRAH silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix forming domain of Sarrah show an increase in apoptosis. One of the direct SARRAH targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability. Overexpression of Sarrah in mice shows better recovery of cardiac contractile function after AMI compared to control mice. In summary, we identified the anti-apoptotic evolutionary conserved lncRNA Sarrah, which is downregulated by aging, as a regulator of cardiomyocyte survival.

Indexed as

ApoptosisAgingAnimalsCarrier ProteinsCell SurvivalCoenzyme A-TransferasesDisease Models, AnimalGene SilencingHumansLIM Domain ProteinsMaleMiceMice, Inbred C57BLMyocardial InfarctionMyocytes, CardiacNF-E2-Related Factor 23-ketoacid CoA-transferaseCarrier ProteinsCoenzyme A-TransferasesCrip2 protein, mouseLIM Domain ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2p300-CBP Transcription FactorsRNA, AntisenseRNA, Long NoncodingRNA, Small Interfering

Identifiers

PMID32341350
PMCPMC7184724
OpenAlexW3018480377

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.