Evidence map›Paper›PMID 9199566›Full record

ArticleAmerican journal of human genetics1997

Haplotypes of angiotensinogen in essential hypertension.

X Jeunemaitre, I Inoue, C Williams, A Charru, J Tichet, M Powers, A M Sharma, A P Gimenez-Roqueplo, A Hata, P Corvol and 1 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in American journal of human genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00857844 (Genetic Predisposition of Chronic Nephrotoxicity From Calcineurin Inhibitors in Liver Transplant Recipients, Potential Correlation With Urinary Biomarkers), which is not on this map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
12.8field-weighted citation impact, top 1% 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.

NCT00857844 completednot on this mapstarted 2007, after this paper: background citation

Genetic Predisposition of Chronic Nephrotoxicity From Calcineurin Inhibitors in Liver Transplant Recipients, Potential Correlation With Urinary Biomarkers

TypeobservationalSponsorNorthwestern UniversityRan2007 to 2012Enrolled207ConditionsComplication of Transplanted Liver
3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 288 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Angiotensinogen as a Therapeutic Target for Cardiovascular and Metabolic Diseases.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  5. Review
  6. Observational
  7. Article
  8. Article
  9. Article
  10. Article
  11. Observational
  12. Article
  13. Association between angiotensinogen M235T polymorphism and hypertrophic cardiomyopathy.International journal of clinical and experimental medicine · 2015
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 6 institutions in 4 countries.

X JeunemaitreLaboratoire de Génétique Moléculaire Hôpital Broussais, Paris, France. jeunemaitre@hbrousssais.fr
I Inoue
C Williams
A Charru
J Tichet
M Powers
A M Sharma
A P Gimenez-Roqueplo
A Hata
P Corvol
J M Lalouel
Howard Hughes Medical Institute · USInserm · FRCollège de France · FRFreie Universität Berlin · DEHokkaido University · JPInstitut de Recherche en Santé, Environnement et Travail · FR

Funding

NHLBI NIH HHS HL-45235
6 · The paper itself

Abstract

The M235T polymorphism of the angiotensinogen gene (AGT) has been associated with essential and pregnancy-induced hypertension. Generation of haplotypes can help to resolve whether the T235 allele itself predisposes to the development of hypertension or acts as a marker of an unknown causal molecular variant. We identified 10 diallelic polymorphisms at the AGT locus and genotyped both a series of 477 probands of hypertensive families and 364 controls, all French Caucasians, as well as a series of 92 hypertensives and 122 controls from Japan. Despite a large ethnic difference in gene frequency, a significant association of T235 with hypertension was observed both in Cancasians (.46 vs. .38, P = .004) and in Japanese (.91 vs. .76, P = .002). In both groups, the G-->A substitution located at position -6 upstream of the initial transcription site occurred at the same frequency and in complete linkage disequilibrium with the T235 allele. No other polymorphism was found to be consistently associated with hypertension. Five informative haplotypes subdividing the T235 allele were generated. Whereas two of them were associated with hypertension in Caucasians, none of these two haplotypes (H3 and H4) reached statistical significance in Japanese. The analysis of the AGT-GT repeat revealed marked linkage disequilibriums between each of the diallelic polymorphisms and some (GT)n alleles, with similar patterns in the two populations. The strong disequilibrium between M235 and (GT)16 explained the increased frequency of that particular allele in French controls compared with hypertensives (.42 vs. .36, P < .01). The haplotype combining the M235T and G-6A polymorphisms appears as the ancestral allele of the human AGT gene and as the one associated with hypertension.

Indexed as

HaplotypesAge of OnsetAngiotensinogenDatabases, FactualDNA PrimersExonsFemaleFranceGene FrequencyGenetic VariationGenotypeHumansHypertensionJapanMaleMiddle AgedAngiotensinogenDNA Primers

Identifiers

PMID9199566
PMCPMC1716122
OpenAlexW1991313384

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Registered trials

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.