Evidence map›Paper›PMID 32783656›Full record

ArticleAmerican journal of physiology. Cell physiology2020

A hypertension patient-derived iPSC model demonstrates a role for G protein-coupled estrogen receptor in hypertension risk and development.

Natalie C Fredette, Eliyah Malik, Marah L Mukhtar, Eric R Prossnitz, Naohiro Terada

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Natalie C FredetteDepartment of Pathology, Immunology and Experimental Medicine, University of Florida College of Medicine, Gainesville, Florida.
Eliyah MalikDepartment of Pathology, Immunology and Experimental Medicine, University of Florida College of Medicine, Gainesville, Florida.
Marah L MukhtarDepartment of Mechanical & Aerospace Engineering, University of Florida Herbert Wertheim College of Engineering, Gainesville, Florida.
Eric R ProssnitzDepartment of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
Naohiro TeradaDepartment of Pathology, Immunology and Experimental Medicine, University of Florida College of Medicine, Gainesville, Florida.
University of Florida · USFlorida College · USUniversity of New Mexico · US

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
Using social networks to map and evaluate team science across CTSA hubsUL1TR001427 · NCATS · UNIVERSITY OF FLORIDA · PI MITCHELL, DUANE A. · 2015 to 2024
$37.2M
Unfolded Protein Response and Autophagy in T Helper Cell Effector FunctionP20GM121176 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Monica Rosas Lemus · 2017 to 2026
$24.9M
Molecular Mechanisms and Applications of Novel ER/GPER-selective LigandsR01CA194496 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI ARTERBURN, JEFFREY B, PROSSNITZ, ERIC R · 2016 to 2025
$4.1M
G protein-coupled estrogen receptor GPER and breast carcinogenesisR01CA163890 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI PROSSNITZ, ERIC R · 2012 to 2023
$3.3M
Training Program in Regenerative MedicineT32DK074367 · NIDDK · UNIVERSITY OF FLORIDA · PI SCOTT, EDWARD W · 2007 to 2022
$2.9M
HHS | National Institutes of Health (NIH) DK104194HHS | National Institutes of Health (NIH) GM119977NCATS NIH HHS UL1 TR001427NCI NIH HHS P30 CA118100NCI NIH HHS R01 CA163890NCI NIH HHS R01 CA194496NIDDK NIH HHS T32 DK074367NIGMS NIH HHS P20 GM121176Univ of FL Clinical and Translational Sicences Institute UL1TR001427
6 · The paper itself

Abstract

Hypertension (HTN) is a polyfactorial disease that can manifest severe cardiovascular pathologies such as heart failure or stroke. Genome-wide association studies (GWAS) of HTN indicate that single-nucleotide polymorphisms (SNPs) contribute to increased risk for HTN and resistance to some HTN drug regimens (Hiltunen TP et al.,

Indexed as

Polymorphism, Single NucleotideAdultAntigens, CDBase SequenceCadherin 5CadherinsCell AdhesionCell DifferentiationCell EngineeringCRISPR-Cas SystemsEndothelial CellsFemaleGene EditingGene Expression RegulationHumansHypertensionAntigens, CDCadherin 5CadherinsGPER1 protein, humanNitric OxideNitric Oxide Synthase Type IIINOS3 protein, humanPECAM1 protein, humanPlatelet Endothelial Cell Adhesion Molecule-1Receptors, EstrogenReceptors, G-Protein-Coupledvon Willebrand FactorendothelialGPERhypertensioniPSCsingle-nucleotide polymorphism

Identifiers

PMID32783656
PMCPMC7701270
OpenAlexW3048872422

What OpenQuestion 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 OpenQuestion graph.