Evidence map›Paper›PMID 18420946›Full record

ArticleCirculation research2008

A cyclin D2-Rb pathway regulates cardiac myocyte size and RNA polymerase III after biomechanical stress in adult myocardium.

Ekaterini Angelis, Alejandro Garcia, Shing S Chan, Katja Schenke-Layland, Shuxen Ren, Sarah J Goodfellow, Maria C Jordan, Kenneth P Roos, Robert J White, W Robb MacLellan

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2008. 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 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Article
  5. Repressive histone methylation regulates cardiac myocyte cell cycle exit.Journal of molecular and cellular cardiology · 2018
    Article
  6. Cyclin D2 is a critical mediator of exercise-induced cardiac hypertrophy.Experimental biology and medicine (Maywood, N.J.) · 2017
    Article
  7. Article
  8. Article
  9. Article
  10. Cyclin D2 is a GATA4 cofactor in cardiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  11. Article
  12. Article
  13. Article
  14. Cyclin D2 rescues size and function of GATA4 haplo-insufficient hearts.American journal of physiology. Heart and circulatory physiology · 2012
    Article
  15. Article
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  19. Article
  20. Novel markers of left ventricular hypertrophy in uremia.American journal of nephrology · 2010
    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

10 authors at 1 institution in 2 countries.

Ekaterini AngelisThe Cardiovascular Research Laboratory, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1760, USA.
Alejandro Garcia
Shing S Chan
Katja Schenke-Layland
Shuxen Ren
Sarah J Goodfellow
Maria C Jordan
Kenneth P Roos
Robert J White
W Robb MacLellan
University of Wisconsin–Madison · US

Funding

ROLE OF P38 MAPK AND PP2C IN ISCHEMIC INJURY AND PROTECTIONP01HL080111 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WEISS, JAMES N · 2005 to 2009
$11.6M
Genetic Dissection of Cardiac Growth: The Role of c-MycR01HL070748 · NHLBI · UNIVERSITY OF WASHINGTON · PI MACLELLAN, WILLIAM ROBB · 2004 to 2020
$5.0M
NHLBI NIH HHS P01 HL080111NHLBI NIH HHS R01 HL070748NHLBI NIH HHS R01 HL70748
6 · The paper itself

Abstract

Normally, cell cycle progression is tightly coupled to the accumulation of cell mass; however, the mechanisms whereby proliferation and cell growth are linked are poorly understood. We have identified cyclin (Cyc)D2, a G(1) cyclin implicated in mediating S phase entry, as a potential regulator of hypertrophic growth in adult post mitotic myocardium. To examine the role of CycD2 and its downstream targets, we subjected CycD2-null mice to mechanical stress. Hypertrophic growth in response to transverse aortic constriction was attenuated in CycD2-null compared with wild-type mice. Blocking the increase in CycD2 in response to hypertrophic agonists prevented phosphorylation of CycD2-target Rb (retinoblastoma gene product) in vitro, and mice deficient for Rb had potentiated hypertrophic growth. Hypertrophic growth requires new protein synthesis and transcription of tRNA genes by RNA polymerase (pol) III, which increases with hypertrophic signals. This load-induced increase in RNA pol III activity is augmented in Rb-deficient hearts. Rb binds and represses Brf-1 and TATA box binding protein (TBP), subunits of RNA pol III-specific transcription factor B, in adult myocardium under basal conditions. However, this association is disrupted in response to transverse aortic constriction. RNA pol III activity is unchanged in CycD2(-/-) myocardium after transverse aortic constriction, and there is no dissociation of TBP from Rb. These investigations identify an essential role for the CycD2-Rb pathway as a governor of cardiac myocyte enlargement in response to biomechanical stress and, more fundamentally, as a regulator of the load-induced activation of RNA pol III.

Indexed as

Age FactorsAnimalsCardiomegalyCells, CulturedCell SizeCyclin D2CyclinsDisease Models, AnimalE2F1 Transcription FactorE2F3 Transcription FactorE2F4 Transcription FactorE2F5 Transcription FactorMiceMice, Mutant StrainsMyocardiumMyocytes, CardiacCcnd2 protein, mouseCyclin D2CyclinsE2f1 protein, mouseE2F1 Transcription FactorE2f3 protein, mouseE2F3 Transcription FactorE2f4 protein, mouseE2F4 Transcription FactorE2f5 protein, mouseE2F5 Transcription FactorRetinoblastoma ProteinRNA Polymerase III

Identifiers

PMID18420946
PMCPMC2447867
OpenAlexW2138944165

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.