Evidence map›Paper›PMID 27725247›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2017

Cardiomyocyte-specific deletion of the G protein-coupled estrogen receptor (GPER) leads to left ventricular dysfunction and adverse remodeling: A sex-specific gene profiling analysis.

Hao Wang, Xuming Sun, Jeff Chou, Marina Lin, Carlos M Ferrario, Gisele Zapata-Sudo, Leanne Groban

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Aromatase enzyme: Paving the way for exploring aromatization for cardio-renal protection.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
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  12. The Effect of Aldosterone on Cardiorenal and Metabolic Systems.International journal of molecular sciences · 2023
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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

7 authors at 2 institutions in 2 countries.

Hao WangDepartment of Anesthesiology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA; Internal Medicine/Molecular Medicine, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA. Electronic address: haowang@wakehealth.edu.
Xuming SunDepartment of Anesthesiology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA.
Jeff ChouPublic Health Sciences, Section on Biostatistical Sciences, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA.
Marina LinDepartment of Anesthesiology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA.
Carlos M FerrarioDepartment of Surgery, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA; Department of Internal Medicine/Nephrology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA.
Gisele Zapata-SudoDepartment of Anesthesiology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA; Institute of Biomedical Sciences, Drug Development Program, Federal University of Rio de Janeiro, Brazil.
Leanne GrobanDepartment of Anesthesiology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA; Internal Medicine/Molecular Medicine, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA; Cardiovascular Research Center, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA; Sticht Center on Aging, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, North Carolina 27157, USA. Electronic address: lgroban@wakehealth.edu.
Wake Forest University · USUniversidade Federal do Rio de Janeiro · BR

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DELL'ITALIA, LOUIS J. · 1994 to 2019
$34.8M
Interplay Between Estrogen, GPR30 and Chymase/RAS in Diastolic FunctionR01AG033727 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 2009 to 2017
$2.8M
The conditional GPR30 knockout mouse: a model of female-specific cardiac agingR03AG042758 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 2012 to 2013
$144k
NHLBI NIH HHS P01 HL051952NIA NIH HHS R01 AG033727NIA NIH HHS R03 AG042758Wellcome Trust
6 · The paper itself

Abstract

Activation of G protein-coupled estrogen receptor (GPER) by its agonist, G1, protects the heart from stressors such as pressure-overload, ischemia, a high-salt diet, estrogen loss, and aging, in various male and female animal models. Due to nonspecific effects of G1, the exact functions of cardiac GPER cannot be concluded from studies using systemic G1 administration. Moreover, global knockdown of GPER affects glucose homeostasis, blood pressure, and many other cardiovascular-related systems, thereby confounding interpretation of its direct cardiac actions. We generated a cardiomyocyte-specific GPER knockout (KO) mouse model to specifically investigate the functions of GPER in cardiomyocytes. Compared to wild type mice, cardiomyocyte-specific GPER KO mice exhibited adverse alterations in cardiac structure and impaired systolic and diastolic function, as measured by echocardiography. Gene deletion effects on left ventricular dimensions were more profound in male KO mice compared to female KO mice. Analysis of DNA microarray data from isolated cardiomyocytes of wild type and KO mice revealed sex-based differences in gene expression profiles affecting multiple transcriptional networks. Gene Set Enrichment Analysis (GSEA) revealed that mitochondrial genes are enriched in GPER KO females, whereas inflammatory response genes are enriched in GPER KO males, compared to their wild type counterparts of the same sex. The cardiomyocyte-specific GPER KO mouse model provides us with a powerful tool to study the functions of GPER in cardiomyocytes. The gene expression profiles of the GPER KO mice provide foundational information for further study of the mechanisms underlying sex-specific cardioprotection by GPER.

Indexed as

Gene DeletionGene Expression ProfilingGene Expression RegulationVentricular Dysfunction, LeftAnimalsFemaleMaleMiceMice, KnockoutMyocytes, CardiacReceptors, EstrogenReceptors, G-Protein-CoupledSex CharacteristicsVentricular RemodelingGPER1 protein, mouseReceptors, EstrogenReceptors, G-Protein-CoupledCardiomyocyteGPERKnockoutMicroarray

Identifiers

PMID27725247
PMCPMC5385168
OpenAlexW2529930616

What OpenQuestion holds

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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.