Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.1002/jcp.24404

http://scihub22266oqcxt.onion/10.1002/jcp.24404
suck pdf from google scholar
C4040522!4040522 !23702776
unlimited free pdf from europmc23702776
    free
PDF from PMC    free
html from PMC    free

Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23702776 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215

suck abstract from ncbi

pmid23702776
      J+Cell+Physiol 2013 ; 228 (12 ): 2337-42
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • SWI/SNF chromatin remodeling enzymes are associated with cardiac hypertrophy in a genetic rat model of hypertension #MMPMID23702776
  • Mehrotra A ; Joe B ; de la Serna IL
  • J Cell Physiol 2013[Dec]; 228 (12 ): 2337-42 PMID23702776 show ga
  • 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.
  • |Animals [MESH]
  • |Cardiomegaly/genetics/*physiopathology [MESH]
  • |Chromatin Assembly and Disassembly/genetics/*physiology [MESH]
  • |Chromosomal Proteins, Non-Histone/*genetics/*metabolism [MESH]
  • |Disease Models, Animal [MESH]
  • |Gene Expression [MESH]
  • |Histones/genetics/metabolism [MESH]
  • |Hypertension/genetics/metabolism/*physiopathology [MESH]
  • |Male [MESH]
  • |Promoter Regions, Genetic [MESH]
  • |Rats [MESH]
  • |Rats, Inbred Dahl/genetics/metabolism/physiology [MESH]
  • |Sodium Chloride, Dietary/metabolism [MESH]
  • |Transcription Factors/*genetics/*metabolism [MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box