Evidence map›Paper›PMID 30988323›Full record

ArticleScientific reports2019

Functional Screening Identifies MicroRNAs as Multi-Cellular Regulators of Heart Failure.

Robin Verjans, Wouter J A Derks, Kerstin Korn, Birte Sönnichsen, Rick E W van Leeuwen, Blanche Schroen, Marc van Bilsen, Stephane Heymans

Abstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–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

24 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. MicroRNAs as therapeutic targets in cardiovascular disease.The Journal of clinical investigation · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Cardiac fibrosis.Cardiovascular research · 2021
    Review
  15. Article
  16. Article
  17. Big Data Approaches in Heart Failure Research.Current heart failure reports · 2020
    Review
  18. Review
  19. 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

8 authors.

Robin VerjansDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6200 MD, Maastricht, Limburg, The Netherlands.
Wouter J A DerksDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6200 MD, Maastricht, Limburg, The Netherlands.
Kerstin KornFormer Cenix BioScience GmbH, 01307, Dresden, Saxony, Germany.
Birte SönnichsenFormer Cenix BioScience GmbH, 01307, Dresden, Saxony, Germany.
Rick E W van LeeuwenDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6200 MD, Maastricht, Limburg, The Netherlands.
Blanche SchroenDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6200 MD, Maastricht, Limburg, The Netherlands.
Marc van BilsenDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6200 MD, Maastricht, Limburg, The Netherlands.
Stephane HeymansDepartment of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6200 MD, Maastricht, Limburg, The Netherlands. s.heymans@maastrichtuniversity.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) is the leading cause of death in the Western world. Pathophysiological processes underlying HF development, including cardiac hypertrophy, fibrosis and inflammation, are controlled by specific microRNAs (miRNAs). Whereas most studies investigate miRNA function in one particular cardiac cell type, their multicellular function is poorly investigated. The present study probed 194 miRNAs -differentially expressed in cardiac inflammatory disease - for regulating cardiomyocyte size, cardiac fibroblasts collagen content, and macrophage polarization. Of the tested miRNAs, 13%, 26%, and 41% modulated cardiomyocyte size, fibroblast collagen production, and macrophage polarization, respectively. Seventeen miRNAs affected all three cellular processes, including miRNAs with established (miR-210) and unknown roles in cardiac pathophysiology (miR-145-3p). These miRNAs with a multi-cellular function commonly target various genes. In-depth analysis in vitro of previously unstudied miRNAs revealed that the observed phenotypical alterations concurred with changes in transcript and protein levels of hypertrophy-, fibrosis- and inflammation-related genes. MiR-145-3p and miR-891a-3p were identified to regulate the fibrotic response, whereas miR-223-3p, miR-486-3p, and miR-488-5p modulated macrophage activation and polarisation. In conclusion, miRNAs are multi-cellular regulators of different cellular processes underlying cardiac disease. We identified previously undescribed roles of miRNAs in hypertrophy, fibrosis, and inflammation, and attribute new cellular effects to various well-known miRNAs.

Indexed as

AnimalsAnimals, NewbornCardiomegalyCells, CulturedFibroblastsFibrosisGene Expression ProfilingGene Expression RegulationHeart FailureHumansMacrophage ActivationMacrophagesMiceMicroRNAsMyocarditisMyocardiumMicroRNAs

Identifiers

PMID30988323
PMCPMC6465262

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.