Evidence map›Paper›PMID 22153880›Full record

ReviewGender medicine2011

Evidence that the G protein-coupled membrane receptor GPR30 contributes to the cardiovascular actions of estrogen.

Sarah H Lindsey, Mark C Chappell

Abstract readReview
In one paragraph

Review in Gender medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Role of GPER in estrogen-dependent nitric oxide formation and vasodilation.The Journal of steroid biochemistry and molecular biology · 2018
    Article
  8. GPER modulators: Opportunity Nox on the heels of a class Akt.The Journal of steroid biochemistry and molecular biology · 2018
    Review
  9. Review
  10. Article
  11. Activation of GPR30 inhibits cardiac fibroblast proliferation.Molecular and cellular biochemistry · 2015
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Sex differences in the pulmonary circulation: implications for pulmonary hypertension.American journal of physiology. Heart and circulatory physiology · 2014
    Review
  17. Review
  18. Article
  19. Sexual dimorphism: the aging kidney, involvement of nitric oxide deficiency, and angiotensin II overactivity.The journals of gerontology. Series A, Biological sciences and medical sciences · 2012
    Review
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.

Sarah H LindseyHypertension and Vascular Research Center, Wake Forest School of Medicine, Winston-Salem, North Carolina 27157-1032, USA. salindse@wakehealth.edu
Mark C Chappell
Wake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 1994 to 2019
$34.8M
Estrogen, ACE2 and Salt-SensitivityR01HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 2004 to 2008
$1.6M
Vascular Interactions of Estrogen Receptor GPR30 and the Renin-Angiotensin SystemR00HL103974 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI LINDSEY, SARAH H. · 2012 to 2014
$710k
Vascular Interactions of Estrogen Receptor GPR30 and the Renin-Angiotensin SystemK99HL103974 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LINDSEY, SARAH H. · 2011 to 2011
$97k
REGULATION AND FUNCTION OF ANGIOTENSIN (1-7)R29HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 1996 to 1999
–
NHLBI NIH HHS HL103974NHLBI NIH HHS HL51952NHLBI NIH HHS HL56973NHLBI NIH HHS K99 HL103974NHLBI NIH HHS P01 HL051952NHLBI NIH HHS R00 HL103974NHLBI NIH HHS R01 HL056973NHLBI NIH HHS R29 HL056973
6 · The paper itself

Abstract

Although female protection from cardiovascular diseases declines with the fall in circulating sex hormones experienced during menopause, clinical trials in older women fail to demonstrate beneficial effects for hormone replacement therapy. The recent discovery of GPR30, a membrane-bound estrogen receptor that is structurally and functionally unique from the steroid receptors ERα and ERβ, has unveiled additional signaling pathways by which estrogen may influence cardiovascular health. This review takes an organ-based approach to assess the expression and function of GPR30 in the cardiovascular system. We concluded that although the current literature does suggest a cardiovascular role for GPR30, additional exploration is necessary to fully elucidate the estrogenic actions mediated by this novel receptor.

Indexed as

AnimalsCardiovascular Physiological PhenomenaCardiovascular SystemEstradiolEstrogen Replacement TherapyEstrogensFemaleHumansReceptors, EstrogenReceptors, G-Protein-CoupledSignal TransductionWomen's HealthEstradiolEstrogensGPER1 protein, humanReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID22153880
PMCPMC3240864
OpenAlexW1993281353

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.