Evidence map›Paper›PMID 21742056›Full record

ReviewVascular pharmacology

The G protein-coupled estrogen receptor GPER/GPR30 as a regulator of cardiovascular function.

Matthias R Meyer, Eric R Prossnitz, Matthias Barton

Registry-linked trialAbstract readReview
In one paragraph

Review in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02558426 (Molecular Analysis of Estrogen Receptors in Patients With Chronic Venous Disease), which is not on this map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
9.6field-weighted citation impact, top 2% 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.

NCT02558426 completednot on this map

Molecular Analysis of Estrogen Receptors in Patients With Chronic Venous Disease

TypeobservationalSponsorUniversity of CatanzaroRan2015 to 2015Enrolled40ConditionsEstrogen Excess, Varicose VeinsArmsVenous Surgery
3 · Its place in the literature

Who cites it

63 citing papers in PubMed, 153 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. GPER-dependent estrogen signaling increases cardiac GCN5L1 expression.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  9. Estrogen-Induced Uterine Vasodilation in Pregnancy and Preeclampsia.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Role of pregnancy hormones and hormonal interaction on the maternal cardiovascular system: a literature review.Clinical research in cardiology : official journal of the German Cardiac Society · 2019
    Review
  20. Review

3 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Matthias R MeyerMolecular Internal Medicine, University of Zurich, Zurich, Switzerland.
Eric R Prossnitz
Matthias Barton
University of Zurich · CHUniversity of New Mexico · US

Funding

Development of GPR30-Selective LigandsR01CA127731 · NCI · UNIVERSITY OF NEW MEXICO · PI ARTERBURN, JEFFREY B, OPREA, TUDOR I · 2008 to 2012
$1.7M
A novel intracellular 7TM estrogen receptor in breastR01CA116662 · NCI · UNIVERSITY OF NEW MEXICO · PI PROSSNITZ, ERIC R · 2006 to 2010
$1.3M
The Role of GPR30 in Advanced Endometrial CancerR01CA118743 · NCI · UNIVERSITY OF NEW MEXICO · PI PROSSNITZ, ERIC R · 2007 to 2009
$855k
NCI NIH HHS CA116662NCI NIH HHS CA118743NCI NIH HHS CA127731NCI NIH HHS R01 CA116662NCI NIH HHS R01 CA118743NCI NIH HHS R01 CA127731
6 · The paper itself

Abstract

Endogenous estrogens are important regulators of cardiovascular homeostasis in premenopausal women and delay the development of hypertension and coronary artery disease. These hormones act via three different estrogen receptors affecting both gene transcription and rapid signaling pathways in a complex interplay. In addition to the classical estrogen receptors ERα and ERβ, which are known mediators of estrogen-dependent vascular effects, a G protein-coupled estrogen receptor termed GPER that is expressed in the cardiovascular system has recently been identified. Endogenous human 17β-estradiol, selective estrogen receptor modulators (SERMs) including tamoxifen and raloxifene, and selective estrogen receptor downregulators (SERDs) such as ICI 182,780 are all agonists of GPER, which has been implicated in the regulation of vasomotor tone and protection from myocardial ischemia/reperfusion injury. As a result, understanding the individual role of ERα, ERβ, and GPER in cardiovascular function has become increasingly complex. With accumulating evidence that GPER is responsible for a variety of beneficial cardiovascular effects of estrogens, this receptor may represent a novel target to develop effective strategies for the treatment of cardiovascular diseases by tissue-specific, selective activation of estrogen-dependent molecular pathways devoid of side effects seen with conventional hormone therapy.

Indexed as

Cardiovascular Physiological PhenomenaAnimalsCardiovascular SystemHumansReceptors, EstrogenReceptors, G-Protein-CoupledReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID21742056
PMCPMC3216677
OpenAlexW2070023795

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.