Evidence map›Paper›PMID 26969820›Full record

ReviewBiochimica et biophysica acta2016

Epigenetic and lncRNA regulation of cardiac pathophysiology.

Ching-Pin Chang, Pei Han

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Long non-coding RNAs: the tentacles of chromatin remodeler complexes.Cellular and molecular life sciences : CMLS · 2021
    Review
  11. Review
  12. LncRNAs Target Ferroptosis-Related Genes and Impair Activation of CD4Frontiers in cell and developmental biology · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Emerging role of lncRNAs in the normal and diseased intestinal barrier.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Review
  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

2 authors at 1 institution in 1 country.

Ching-Pin ChangKrannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Department of Biochemistry and Molecular Biology, Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA. Electronic address: changcp@iu.edu.
Pei HanKrannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Department of Biochemistry and Molecular Biology, Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Indiana University School of Medicine

Funding

LncRNA mechanism of heart failureR01HL121197 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CHANG, CHING-PIN · 2014 to 2022
$3.8M
Chromatin mechanism of molecular motor gene regulationR01HL118087 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CHANG, CHING-PIN · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL118087NHLBI NIH HHS R01HL118087NHLBI NIH HHS R01 HL121197NHLBI NIH HHS R01HL121197
6 · The paper itself

Abstract

Our developmental studies provide an insight into the pathogenesis of heart failure in adults. These studies reveal a mechanistic link between fetal cardiomyocytes and pathologically stressed adult cardiomyocytes at the level of chromatin regulation. In embryos, chromatin-regulating factors within the cardiomyocytes respond to developmental signals to program cardiac gene expression to promote cell proliferation and inhibit premature cell differentiation. In the neonatal period, the activity of these developmental chromatin regulators is quickly turned off in cardiomyocytes, coinciding with the cessation of cell proliferation and advance in cell differentiation toward adult maturity. When the mature hearts are pathologically stressed, those chromatin regulators essential for cardiomyocyte development in embryos are reactivated, triggering gene reprogramming to a fetal-like state and pathological cardiac hypertrophy. Furthermore, in the study of chromatin regulation and cardiac gene expression, we identified a long noncoding RNA that interacts with chromatin remodeling factor to regulate the cardiac response to environmental changes. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel.

Indexed as

Epigenesis, GeneticMyocytes, CardiacAnimalsChromatin Assembly and DisassemblyDNA HelicasesGene-Environment InteractionGene Expression RegulationGenetic Predisposition to DiseaseHeart DiseasesHumansNuclear ProteinsPhenotypeRisk FactorsRNA, Long NoncodingSignal TransductionTranscription FactorsDNA HelicasesNuclear ProteinsRNA, Long NoncodingSMARCA4 protein, humanTranscription FactorsBAFBrg1ChromatinDevelopmentGene expressionHeart failureHypertrophyMhrtMyheart

Identifiers

PMID26969820
PMCPMC7393981
OpenAlexW2293946349

What OpenQuestion holds

Textmetadata
LicenceTDM
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.