Evidence map›Paper›PMID 38872760›Full record

ArticleChronic diseases and translational medicine2024

Analysis of the combined effect of rs699 and rs5051 on angiotensinogen expression and hypertension.

Nicholas R Powell, Tyler Shugg, Jacob Leighty, Matthew Martin, Rolf P Kreutz, Michael T Eadon, Dongbing Lai, Tao Lu, Todd C Skaar

Abstract read
In one paragraph

Article in Chronic diseases and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Nicholas R PowellDivision of Clinical Pharmacology, Department of Medicine School of Medicine, Indiana University Indianapolis Indiana USA.ORCID 0000-0003-4572-0733
Tyler ShuggDivision of Clinical Pharmacology, Department of Medicine School of Medicine, Indiana University Indianapolis Indiana USA.
Jacob LeightyDivision of Clinical Pharmacology, Department of Medicine School of Medicine, Indiana University Indianapolis Indiana USA.
Matthew MartinDepartment of Pharmacology and Toxicology School of Medicine, Indiana University Indianapolis Indiana USA.
Rolf P KreutzDepartment of Cardiology School of Medicine, Krannert Institute of Cardiology, Indiana University Indianapolis Indiana USA.
Michael T EadonDivision of Nephrology, Department of Medicine School of Medicine, Indiana University Indianapolis Indiana USA.
Dongbing LaiDepartment of Medical and Molecular Genetics School of Medicine, Indiana University Indianapolis Indiana USA.
Tao LuDepartment of Pharmacology and Toxicology School of Medicine, Indiana University Indianapolis Indiana USA.
Todd C SkaarDivision of Clinical Pharmacology, Department of Medicine School of Medicine, Indiana University Indianapolis Indiana USA.

Funding

Indiana University Comprehensive Training in Clinical PharmacologyT32GM008425 · NIGMS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Zeruesenay Desta, Michael Thomas Eadon · 1992 to 2026
$7.7M
EXTRAMURAL RESEARCH FACILITIES IMPROVEMENT: NEUROLOGICAL DISORDERS:ALZ, PDC06RR020128 · NCRR · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIFE, ROSE S · 2004 to 2004
$3.7M
MIRA-Regulation of drug metabolizing enzymesR35GM131812 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI SKAAR, TODD C. · 2019 to 2023
$2.5M
Gene-specific responses to NF-kB through lysine and arginine methylation of p65R01GM120156 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI LU, TAO · 2017 to 2021
$1.5M
Investigation of the Immune-Mediated Drug-Drug Interaction Potential of Immune Checkpoint InhibitorsK23GM147805 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI Tyler A Shugg · 2022 to 2026
$836k
Impact of NF-kB methylation on chemoresistance and metastasis of breast cancerR03CA223906 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI LU, TAO, NAKSHATRI, HARIKRISHNA · 2018 to 2019
$157k
NCI NIH HHS R03 CA223906NCRR NIH HHS C06 RR020128NIGMS NIH HHS K23 GM147805NIGMS NIH HHS L30 GM151735NIGMS NIH HHS R01 GM120156NIGMS NIH HHS R35 GM131812NIGMS NIH HHS T32 GM008425
6 · The paper itself

Abstract

Background: Hypertension (HTN) involves genetic variability in the renin-angiotensin system and influences antihypertensive response. We previously reported that angiotensinogen ( Methods: We used in silico, in vitro, in vivo, and retrospective models to test this hypothesis. Results: In silico, rs699 A > G is predicted to increase miR-122-5p binding affinity by 3%. Mir-eCLIP results show rs699 is 40-45 nucleotides from the strongest microRNA-binding site in the Conclusions: We found that rs5051 C > T and rs699 A > G significantly associate with systolic blood pressure in Black participants in the UK Biobank, demonstrating a fourfold larger effect than in White participants. Further studies are warranted to determine if altered antihypertensive response in Black individuals might be due to rs5051 C > T or rs699 A > G. Studies like this will help clinicians move beyond the use of race as a surrogate for genotype.

Indexed as

angiotensinogengenetic and genomic medicinehypertensionrs699

Identifiers

PMID38872760
PMCPMC11166681

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Registered trials

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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.