Evidence map›Paper›PMID 40552363›Full record

ArticleJournal of hypertension2025

Genome-wide association study of angiotensinogen levels and key single nucleotide polymorphism associations with blood pressure.

Karita C F Lidani, Shubham Tomar, Hossein Mousavi, Robert Buscaglia, Kirolos Michael, Alexander P Landry, Leonie Dupuis, Erin D Michos, Erin S Morgan, Xiuqing Guo and 7 more

Abstract read
In one paragraph

Article in Journal of hypertension, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
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

17 authors.

Karita C F LidaniDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Shubham TomarDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Hossein MousaviDepartment of Chemistry and Biochemistry, New Mexico State University, Las Cruces, New Mexico.
Robert BuscagliaDepartment of Mathematics and Statistics, Northern Arizona University, Flagstaff, Arizona.
Kirolos MichaelDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Alexander P LandryDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Leonie DupuisDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Erin D MichosDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Erin S MorganIonis Pharmaceuticals, Carlsbad.
Xiuqing GuoThe Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance.
Jie YaoThe Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance.
Henry J LinThe Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance.
Jerome I RotterThe Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance.
Wendy S PostDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Sotirios TsimikasIonis Pharmaceuticals, Carlsbad.
Patrick J TrainorDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Andrew P DeFilippisDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Funding

NM-INBRE Sequencing and Bioinformatics CoreP20GM103451 · NIGMS · NEW MEXICO STATE UNIVERSITY LAS CRUCES · PI Charlotte C. Gard · 2012 to 2026
$61.2M
CHARGE Consortium: Omics Discovery for CVD and Aging PhenotypesR01HL105756 · NHLBI · UNIVERSITY OF WASHINGTON · PI Bruce M Psaty, NICHOLAS L SMITH · 2011 to 2026
$9.5M
Integrated proteomic and metabolomics analysis of thrombotic myocardial infarctionSC1GM139730 · NIGMS · NEW MEXICO STATE UNIVERSITY LAS CRUCES · PI TRAINOR, PATRICK J · 2021 to 2024
$888k
NHLBI NIH HHS R01 HL105756NIGMS NIH HHS P20 GM103451NIGMS NIH HHS SC1 GM139730
6 · The paper itself

Abstract

objectiveThe renin angiotensin aldosterone system plays a key role in circulatory homeostasis. We sought to identify genetic determinants of measured plasma angiotensinogen levels and subsequently evaluate the association of these single nucleotide polymorphisms (SNPs) with blood pressure (BP) and hypertension in a multiethnic population.

methodsGenome-wide association study (GWAS) of plasma angiotensinogen levels, measured using an enzyme-linked immunoassay, was conducted in 4899 Multi-Ethnic Study of Atherosclerosis (MESA) participants (self-identified as White, n = 1865; Hispanic, n  = 1113; Black, n  = 1224; and Chinese, n  = 629). Linear and logistic models examined the association between SNPs with angiotensinogen and hypertension, respectively. Mediation analysis evaluated the effect of angiotensinogen on BP/hypertension through the top SNPs identified by GWAS.

resultsIn the analysis utilizing all participants, 115 SNPs were associated with angiotensinogen ( P  < 5 × 10 -8 ), including lead SNP rs4762(G>A) in exon 2 ( P  = 1.51E -100 ) and rs5050(T>G) in the promoter region ( P  = 2.26E -69 ) of the AGT gene. Race/ethnic-specific analyses identified rs4762(G>A) as the lead SNP for White and Hispanic participants, whereas Black and Chinese participants had rs5050(T>G) and rs16852311(G>C), respectively. Both rs4762(G>A) and rs5050(T>G) indirectly increased systolic BP, diastolic BP, and the odds of hypertension through its effect of increasing angiotensinogen.

conclusionsOur findings demonstrate racial/ethnic differences in genetic effects on angiotensinogen levels across multiple SNPs. AGT rs4762(G>A) and rs5050(T>G) impact BP and hypertension through a mediated effect via angiotensinogen, though opposing direct effects may mask the overall association.

Indexed as

AngiotensinogenBlood PressureGenome-Wide Association StudyHypertensionPolymorphism, Single NucleotideAgedFemaleHumansMaleMiddle AgedAGT protein, humanAngiotensinogenangiotensinogengenome wide association studyhypertension

Identifiers

PMID40552363
PMCPMC12337919

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.