Evidence map›Paper›PMID 20036967›Full record

ReviewFrontiers in bioscience (Scholar edition)2010

Deregulation of RGS2 in cardiovascular diseases.

Sharon Tsang, Anthony Yiu-Ho Woo, Weizhong Zhu, Rui-Ping Xiao

Open access · bronzeAbstract readReview
In one paragraph

Review in Frontiers in bioscience (Scholar edition), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Associations ofPharmaceutics · 2022
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Hypertension in mice with transgenic activation of the brain renin-angiotensin system is vasopressin dependent.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Sharon TsangLaboratory of Cardiovascular Science, National Institute on Aging, Baltimore, MD 21224, USA.
Anthony Yiu-Ho Woo
Weizhong Zhu
Rui-Ping Xiao
National Institute on Aging · US

Funding

Dimerization of Beta1-Adrenergic Receptor with RAGE Induces Heart Cell DeathZIAAG000873 · NIA · NATIONAL INSTITUTE ON AGING · PI ZHU, WEIZHONG · 2009 to 2010
$444k
Agonist Stereochemistry Determines Beta2-Adrenergic G Protein Coupling ZIAAG000871 · NIA · NATIONAL INSTITUTE ON AGING · PI LAKATTA, EDWARD · 2009 to 2010
$422k
RGS2 Constitutes A Negative Regulator of Beta2-Adrenergic Gi SignalingZIAAG000870 · NIA · NATIONAL INSTITUTE ON AGING · PI LAKATTA, EDWARD · 2009 to 2010
$400k
Cardioprotection by CaMKII-dB Is Mediated by Inducible HSP70ZIAAG000287 · NIA · NATIONAL INSTITUTE ON AGING · PI ZHU, WEIZHONG · 2009 to 2010
$388k
Suppression of Beta-arrestin1 Phosphorylation and Function by Beta-arrestin2ZIAAG000862 · NIA · NATIONAL INSTITUTE ON AGING · PI LAKATTA, EDWARD · 2009 to 2010
$377k
Intramural NIH HHS ZIA AG000870
6 · The paper itself

Abstract

Alteration of G protein-coupled receptor (GPCR) signaling is a salient feature of hypertension and the associated heart diseases. Recent studies have revealed a large family of Regulators of G-protein Signaling (RGS) proteins as important endogenous regulators of GPCR signaling. RGS2 selectively regulates Galphaq/11 signaling, an essential cause of hypertension and cardiac hypertrophy. Both clinical and animal studies have shown that deregulation of RGS2 leads to exacerbated Galphaq/11 signaling. There is an inverse correlation between RGS2 expression and blood pressure, as well as a selective down-regulation of RGS2 in various models of cardiac hypertrophy. The causal relationship has been established in animal studies. RGS2 knockout mice exhibit not only hypertension phenotype but also accelerated cardiac hypertrophy and heart failure in response to pressure-overload. Further in vitro studies have shown that RGS2 knockdown with RNA interference exacerbates, whilst RGS2 over-expression completely abolishes the Galphaq/11-induced hypertrophy. These findings indicate that deregulation of RGS2 plays a crucial role in the pathogenesis of cardiovascular diseases, marking RGS2 as a potential therapeutic target or biomarker of hypertension or hypertensive heart diseases.

Indexed as

AnimalsCardiomegalyCardiovascular DiseasesGene Expression RegulationGTP-Binding Protein alpha Subunits, Gq-G11HumansHypertensionMiceMyocardiumRGS ProteinsSignal TransductionGTP-Binding Protein alpha Subunits, Gq-G11RGS2 protein, humanRGS Proteins

Identifiers

PMID20036967
PMCPMC2815333
OpenAlexW2053171883

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.