Evidence map›Paper›PMID 22194017›Full record

ReviewActa biochimica et biophysica Sinica2012

Epigenetic mechanisms in cardiac development and disease.

Marcus Vallaster, Caroline Dacwag Vallaster, Sean M Wu

Open access · greenAbstract readReview
In one paragraph

Review in Acta biochimica et biophysica Sinica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. [Interactive regulatory effect of histone H3K9ac acetylation and histone H3K9me3 methylation on cardiomyogenesis in mice].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Asxl2Journal of developmental biology · 2016
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Epigenetics of the failing heart.Heart failure reviews · 2015
    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

3 authors at 1 institution in 1 country.

Marcus VallasterCardiovascular Research Center, Massachusetts General Hospital, Boston, 02114, USA.
Caroline Dacwag Vallaster
Sean M Wu
Massachusetts General Hospital · US

Funding

MULTIDISCIPLINARY RESEARCH TRAINING IN CARDIOLOGYT32HL007208 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Patrick Thomas Ellinor, David E Sosnovik · 1985 to 2026
$16.1M
Human Pluripotent Stem Cell and Progenitor Models of Cardiac and Blood DiseasesU01HL100408 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI COWAN, CHAD ALBERT, MELTON, DOUGLAS A · 2009 to 2015
$8.9M
Generation of functional organs via developmental chimerismDP2OD004411 · OD · STANFORD UNIVERSITY · PI WU, SEAN M · 2008 to 2008
$2.5M
Cardiac Progenitor Cells in Development and DiseaseK08HL081086 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI WU, SEAN M · 2005 to 2010
$657k
NHLBI NIH HHS 5T32HL007208NHLBI NIH HHS HL081086NHLBI NIH HHS HL100408NHLBI NIH HHS K08 HL081086NIH HHS DP2 OD004411NIH HHS OD004411
6 · The paper itself

Abstract

During mammalian development, cardiac specification and ultimately lineage commitment to a specific cardiac cell type is accomplished by the action of specific transcription factors (TFs) and their meticulous control on an epigenetic level. In this review, we detail how cardiac-specific TFs function in concert with nucleosome remodeling and histone-modifying enzymes to regulate a diverse network of genes required for processes such as cell growth and proliferation, or epithelial to mesenchymal transition (EMT), for instance. We provide examples of how several cardiac TFs, such as Nkx2.5, WHSC1, Tbx5, and Tbx1, which are associated with developmental and congenital heart defects, are required for the recruitment of histone modifiers, such as Jarid2, p300, and Ash2l, and components of ATP-dependent remodeling enzymes like Brg1, Baf60c, and Baf180. Binding of these TFs to their respective sites at cardiac genes coincides with a distinct pattern of histone marks, indicating that the precise regulation of cardiac gene networks is orchestrated by interactions between TFs and epigenetic modifiers. Furthermore, we speculate that an epigenetic signature, comprised of TF occupancy, histone modifications, and overall chromatin organization, is an underlying mechanism that governs cardiac morphogenesis and disease.

Indexed as

Epigenesis, GeneticAbnormalities, MultipleAnimalsCell DifferentiationCHARGE SyndromeChromatinChromosomal Proteins, Non-HistoneDiGeorge SyndromeDNA HelicasesEmbryonic Stem CellsGene Expression Regulation, DevelopmentalHeartHeart Defects, CongenitalHeart Septal Defects, AtrialHomeobox Protein Nkx-2.5Homeodomain ProteinsChromatinChromosomal Proteins, Non-HistoneDNA HelicasesHomeobox Protein Nkx-2.5Homeodomain ProteinsNKX2-5 protein, humanNuclear ProteinsNucleosomesSMARCA4 protein, humanSWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID22194017
PMCPMC3244653
OpenAlexW2152471877

What OpenQuestion holds

Textmetadata
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.