Evidence map›Paper›PMID 29203887›Full record

ArticleScientific reports2017

Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health.

Johanna Heid, Chiara Cencioni, Roberto Ripa, Mario Baumgart, Sandra Atlante, Giuseppina Milano, Alessandro Scopece, Carsten Kuenne, Stefan Guenther, Valerio Azzimato and 9 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

41 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. miRNA family miR-29 inhibits PINK1-PRKN signaling via ATG9A.Molecular neurodegeneration advances · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Role of noncoding RNAs in cardiac ageing.Frontiers in cardiovascular medicine · 2023
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

19 authors at 10 institutions in 5 countries.

Johanna HeidDivision of Cardiovascular Epigenetics, Department of Cardiology, Goethe University, Frankfurt am Main, 60596, Germany.
Chiara CencioniDivision of Cardiovascular Epigenetics, Department of Cardiology, Goethe University, Frankfurt am Main, 60596, Germany.
Roberto RipaScuola Normale Superiore, Laboratory of Biology (Bio@SNS), c/o Istituto di Biofisica del CNR, Pisa, 56124, Italy.
Mario BaumgartLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, 07745, Germany.ORCID 0000-0001-8172-1595
Sandra AtlanteDivision of Cardiovascular Epigenetics, Department of Cardiology, Goethe University, Frankfurt am Main, 60596, Germany.
Giuseppina MilanoVascular Biology and Regenerative Medicine Unit, Centro Cardiologico Monzino-IRCCS, Milan, 20128, Italy.
Alessandro ScopeceVascular Biology and Regenerative Medicine Unit, Centro Cardiologico Monzino-IRCCS, Milan, 20128, Italy.
Carsten KuenneECCPS Bioinformatics and deep sequencing platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Stefan GuentherECCPS Bioinformatics and deep sequencing platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Valerio AzzimatoIntegrated Cardio Metabolic Centre, Department of Medicine, Karolinska Institutet, Huddinge, 141 57, Sweden.
Antonella FarsettiNational Research Council, Institute of Cell Biology and Neurobiology (IBCN), Rome, 00143, Italy.
Giacomo RossiDepartment of Veterinary Sciences, Faculty of Veterinary Medicine, University of Camerino, Camerino, (MC), 62032, Italy.
Thomas BraunECCPS Bioinformatics and deep sequencing platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, 61231, Germany.
Giulio PompilioVascular Biology and Regenerative Medicine Unit, Centro Cardiologico Monzino-IRCCS, Milan, 20128, Italy.
Fabio MartelliIRCCS-Policlinico San Donato, Moleculary Cardiology Laboratory, San Donato Milanese, (MI), 20097, Italy.
Andreas M ZeiherInternal Medicine Clinic III, Department of Cardiology, Goethe University, Frankfurt am Main, 60596, Germany.
Alessandro CellerinoScuola Normale Superiore, Laboratory of Biology (Bio@SNS), c/o Istituto di Biofisica del CNR, Pisa, 56124, Italy.
Carlo GaetanoDivision of Cardiovascular Epigenetics, Department of Cardiology, Goethe University, Frankfurt am Main, 60596, Germany. carlo.gaetano@gmail.com.ORCID 0000-0002-5238-1832
Francesco SpallottaDivision of Cardiovascular Epigenetics, Department of Cardiology, Goethe University, Frankfurt am Main, 60596, Germany. fspallotta@gmail.com.
Goethe University Frankfurt · DEMax Planck Institute for Heart and Lung Research · DECentro Cardiologico Monzino · ITScuola Normale Superiore · ITIRCCS Policlinico San Donato · ITKarolinska Institutet · SELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DENational Research Council · ITUniversità di Camerino · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12-21 week (adult) and 28-40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O

Indexed as

AgingOxidative Stress5-MethylcytosineAnimalsAntagomirsCell HypoxiaCell LineCollagenDNA MethylationEchocardiographyFibroblastsFishesHeartHumansMicroRNAsMyocardium5-MethylcytosineAntagomirsCollagenMicroRNAs

Identifiers

PMID29203887
PMCPMC5715159
OpenAlexW2769166145

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.