Evidence map›Paper›PMID 21778436›Full record

ReviewCirculation research2011

Regulators of G-protein signaling in the heart and their potential as therapeutic targets.

Peng Zhang, Ulrike Mende

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

47 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Article
  3. G protein regulation by RGS proteins in the pathophysiology of dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Role of G-Proteins and GPCRs in Cardiovascular Pathologies.Bioengineering (Basel, Switzerland) · 2023
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. RGS14 Regulation of Post-Synaptic Signaling and Spine Plasticity in Brain.International journal of molecular sciences · 2021
    Review
  20. The association between RGS4 and choline in cardiac fibrosis.Cell communication and signaling : CCS · 2021
    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

2 authors at 1 institution in 1 country.

Peng ZhangCardiovascular Research Center, Rhode Island Hospital and Alpert Medical School of Brown University, 1 Hoppin St, Providence, RI 02903, USA.
Ulrike Mende
Brown University · US

Funding

RGS Regulation of Cardiac Signaling and HypertrophyR01HL080127 · NHLBI · RHODE ISLAND HOSPITAL · PI MENDE, ULRIKE · 2006 to 2010
$1.8M
NHLBI NIH HHS HL-80127NHLBI NIH HHS R01 HL080127
6 · The paper itself

Abstract

Signal transduction through G-protein-coupled receptors (GPCRs) is central for the regulation of virtually all cellular functions and has been widely implicated in human disease. Regulators of G-protein signaling (RGS proteins) belong to a diverse protein family that was originally discovered for their ability to accelerate signal termination in response to GPCR stimulation, thereby reducing the amplitude and duration of GPCR effects. All RGS proteins share a common RGS domain that interacts with G protein α subunits and mediates their biological regulation of GPCR signaling. However, RGS proteins differ widely in size and the organization of their sequences flanking the RGS domain, which contain several additional functional domains that facilitate protein-protein (or protein-lipid) interactions. RGS proteins are subject to posttranslational modifications, and, in addition, their expression, activity, and subcellular localization can be dynamically regulated. Thus, there exists a wide array of mechanisms that facilitate their proper function as modulators and integrators of G-protein signaling. Several RGS proteins have been implicated in the cardiac remodeling response and heart rate regulation, and changes in RGS protein expression and/or function are believed to participate in the pathophysiology of cardiac hypertrophy, failure and arrhythmias as well as hypertension. This review is based on recent advances in our understanding of the expression pattern, regulation, and functional role of canonical RGS proteins, with a special focus on the healthy heart and the diseased heart. In addition, we discuss their potential and promise as therapeutic targets as well as strategies to modulate their expression and function.

Indexed as

Heart DiseasesAnimalsGTP-Binding ProteinsHumansSignal TransductionVentricular RemodelingGTP-Binding Proteins

Identifiers

PMID21778436
PMCPMC3230557
OpenAlexW2165148544

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.