Evidence map›Paper›PMID 22328091›Full record

ArticleCardiovascular research2012

Activation of GPR30 attenuates diastolic dysfunction and left ventricle remodelling in oophorectomized mRen2.Lewis rats.

Hao Wang, Jewell A Jessup, Marina S Lin, Clarissa Chagas, Sarah H Lindsey, Leanne Groban

Abstract read
In one paragraph

Article in Cardiovascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 120 citations in OpenAlex.

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  13. Effect of ovariohysterectomy on queen myocardial function: echocardiographic evidence.Veterinary research forum : an international quarterly journal · 2023
    Article
  14. Life (Basel, Switzerland) · 2022
    Article
  15. Sex differences in vascular aging and impact of GPER deletion.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

14 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

6 authors at 1 institution in 1 country.

Hao WangDepartment of Anesthesiology, Wake Forest School of Medicine, Winston-Salem, Medical Center Boulevard, Winston-Salem, NC 27157-1009, USA.
Jewell A Jessup
Marina S Lin
Clarissa Chagas
Sarah H Lindsey
Leanne Groban
Wake Forest University · US

Funding

Interplay Between Estrogen, GPR30 and Chymase/RAS in Diastolic FunctionR01AG033727 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 2009 to 2017
$2.8M
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
NHLBI NIH HHS K99 HL103974NHLBI NIH HHS R00 HL103974NIA NIH HHS R01-AG033727-03
6 · The paper itself

Abstract

aimsGPR30 is a novel oestrogen receptor expressed in various tissues, including the heart. We determined the role of GPR30 in the maintenance of left ventricular (LV) structure and diastolic function after the surgical loss of ovarian hormones in the female mRen2.Lewis rat, a model emulating the cardiac phenotype of the post-menopausal woman. METHODS AND

resultsBilateral oophorectomy (OVX) or sham surgery was performed in study rats; the selective GPR30 agonist, G-1 (50 µg/kg/day), or vehicle was given subcutaneously to OVX rats from 13-15 weeks of age. Similar to the cardiac phenotype of sham rats, G-1 preserved diastolic function and structure relative to vehicle-treated OVX littermates independent of changes in blood pressure. G-1 limited the OVX-induced increase in LV filling pressure, LV mass, wall thickness, interstitial collagen deposition, atrial natriuretic factor and brain natriuretic peptide mRNA levels, and cardiac NAD(P)H oxidase 4 (NOX4) expression. In vitro studies showed that G-1 inhibited angiotensin II-induced hypertrophy in H9c2 cardiomyocytes, evidenced by reductions in cell size, protein content per cell, and atrial natriuretic factor mRNA levels. The GPR30 antagonist, G15, inhibited the protective effects of both oestradiol and G-1 on this hypertrophy.

conclusionThese data show that the GPR30 agonist G-1 mitigates the adverse effects of oestrogen loss on LV remodelling and the development of diastolic dysfunction in the study rats. This expands our knowledge of the sex-specific mechanisms underlying diastolic dysfunction and provides a potential therapeutic target for reducing the progression of this cardiovascular disease process in post-menopausal women.

Indexed as

OvariectomyAngiotensin IIAnimalsAtrial Natriuretic FactorBlood PressureCalciumCardiotonic AgentsCell LineCollagenCyclopentanesEchocardiography, DopplerEstrogensFemaleGene Expression RegulationGenotypeHypertrophy, Left Ventricular1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanoneAngiotensin IIAtrial Natriuretic FactorCalciumCardiotonic AgentsCollagenCyclopentanesEstrogensGper1 protein, ratNADPH Oxidase 4NADPH OxidasesNatriuretic Peptide, BrainNox4 protein, ratQuinolinesReceptors, G-Protein-CoupledRen2 protein, mouseReninRNA, Messenger

Identifiers

PMID22328091
PMCPMC3307382
OpenAlexW2138650758

What Socratic 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 Socratic graph.