Evidence map›Paper›PMID 23702776›Full record

ArticleJournal of cellular physiology2013

SWI/SNF chromatin remodeling enzymes are associated with cardiac hypertrophy in a genetic rat model of hypertension.

Aanchal Mehrotra, Bina Joe, Ivana L de la Serna

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Histone methylation and vascular biology.Clinical epigenetics · 2020
    Review
  12. Review
  13. Epigenetic modification: a regulatory mechanism in essential hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Epigenetics of the failing heart.Heart failure reviews · 2015
    Review
  19. Article
  20. SWI/SNF chromatin-remodeling complexes in cardiovascular development and disease.Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
    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.

Aanchal MehrotraDepartment of Biochemistry and Cancer Biology, University of Toledo College of Medicine and Life Sciences, Toledo, OH.
Bina Joe
Ivana L de la Serna
University of Toledo · US

Funding

Genetics of HypertensionR01HL020176 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI JOE, BINA · 1985 to 2017
$8.1M
Innovative Models for Mechanistic Studies of Novel Hypertension GenesR01HL112641 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI JOE, BINA · 2012 to 2016
$3.3M
Regulation of Melanocyte Differentiation by SWI/SNF Chromatin Remodeling EnzymesR01AR059379 · NIAMS · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI DE LA SERNA, IVANA L · 2010 to 2014
$1.6M
BIOCHEMISTRY AND GENETICS OF HYPERTENSIONR37HL020176 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI RAPP, JOHN P · 1993 to 2002
$1.6M
NHLBI NIH HHS HL020176NHLBI NIH HHS HL112641NHLBI NIH HHS R01 HL020176NHLBI NIH HHS R01 HL112641NHLBI NIH HHS R37 HL020176NIAMS NIH HHS R01 AR059379PHS HHS ARO59379
6 · The paper itself

Abstract

Pathological cardiac hypertrophy is characterized by a sustained increase in cardiomyocyte size and re-activation of the fetal cardiac gene program. Previous studies implicated SWI/SNF chromatin remodeling enzymes as regulators of the fetal cardiac gene program in surgical models of cardiac hypertrophy. Although hypertension is a common risk factor for developing cardiac hypertrophy, there has not yet been any investigation into the role of SWI/SNF enzymes in cardiac hypertrophy using genetic models of hypertension. In this study, we tested the hypothesis that components of the SWI/SNF complex are activated and recruited to promoters that regulate the fetal cardiac gene program in hearts that become hypertrophic as a result of salt induced hypertension. Utilizing the Dahl salt-sensitive (S) rat model, we found that the protein levels of several SWI/SNF subunits required for heart development, Brg1, Baf180, and Baf60c, are elevated in hypertrophic hearts from S rats fed a high salt diet compared with normotensive hearts from Dahl salt-resistant (R) rats fed the same diet. Furthermore, we detected significantly higher levels of SWI/SNF subunit enrichment as well as evidence of more accessible chromatin structure on two fetal cardiac gene promoters in hearts from S rats compared with R rats. Our data implicate SWI/SNF chromatin remodeling enzymes as regulators of gene expression in cardiac hypertrophy resulting from salt induced hypertension. Thus we provide novel insights into the epigenetic mechanisms by which salt induced hypertension leads to cardiac hypertrophy.

Indexed as

AnimalsCardiomegalyChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneDisease Models, AnimalGene ExpressionHistonesHypertensionMalePromoter Regions, GeneticRatsRats, Inbred DahlSodium Chloride, DietaryTranscriptional ActivationTranscription FactorsChromosomal Proteins, Non-HistoneHistonesSodium Chloride, DietarySWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID23702776
PMCPMC4040522
OpenAlexW1617652799

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.