Evidence map›Paper›PMID 23715995›Full record

ArticleLung2013

Angiotensinogen promoter polymorphisms predict low diffusing capacity in U.S. and Spanish IPF cohorts.

My-Trang T Dang, Chenyang Gu, Jeannie I Klavanian, Katherine A Jernigan, Karen H Friderici, Yuehua Cui, Maria Molina-Molina, Julio Ancochea, Antoni Xaubet, Bruce D Uhal

Abstract readComparative Study
In one paragraph

Article in Lung, 2013. 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
0.5field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
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

10 authors at 4 institutions in 2 countries.

My-Trang T DangDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI, USA.
Chenyang Gu
Jeannie I Klavanian
Katherine A Jernigan
Karen H Friderici
Yuehua Cui
Maria Molina-Molina
Julio Ancochea
Antoni Xaubet
Bruce D Uhal
Michigan State University · USCentro de Investigación Biomédica en Red de Enfermedades Respiratorias · ESHospital Universitario de La Princesa · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

CONTROL OF TYPE II PNEUMOCYTE PROLIFERATIONR01HL045136 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI UHAL, BRUCE D · 1996 to 2012
$2.9M
CONTROL OF TYPE II PNEUMOCYTE PROLIFERATIONR29HL045136 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI UHAL, BRUCE D · 1990 to 1994
–
NHLBI NIH HHS HL-45136NHLBI NIH HHS R01 HL045136
6 · The paper itself

Abstract

backgroundSingle nucleotide polymorphisms (SNPs) in angiotensinogen (AGT) at positions -20 and -6 are associated with increased severity and progression of various fibrotic diseases. Our earlier work demonstrated that the progression of idiopathic pulmonary fibrosis (IPF) was associated with the A-6 allele. This study examined the hypothesis that the homozygous CC genotype at -20 and the AA genotype at -6 would confer worse measures of pulmonary function (measured by pulmonary function tests) in IPF.

methodsMultiple logistic regression analysis was applied to a NIH Lung Tissue Research Consortium cohort and a Spanish cohort, while also adjusting for covariates to determine the effects of these SNPs on measures of pulmonary function.

resultsAnalysis demonstrated that the CC genotype at -20 was strongly associated with reduced diffusing capacity in males in both cohorts (p = 0.0028 for LTRC and p = 0.017 for the Spanish cohort). In females, the AA genotype was significantly associated with lower FVC (p = 0.0082) and V alv (p = 0.022). In males, the haplotype CA at -20 and -6 in AGT was also strongly associated with reduced diffusing capacity in both cohorts.

conclusionsThis study is the first to demonstrate an association of AGT polymorphisms (-20A > C and -6G > A) with lower measures of pulmonary function in IPF. It is also the first to relate the effect of gender in lung fibrosis with polymorphisms in AGT.

Indexed as

Polymorphism, Single NucleotidePromoter Regions, GeneticAgedAngiotensinogenChi-Square DistributionFemaleForced Expiratory VolumeGene FrequencyGenetic Predisposition to DiseaseHaplotypesHomozygoteHumansIdiopathic Pulmonary FibrosisLikelihood FunctionsLogistic ModelsLungAGT protein, humanAngiotensinogen

Identifiers

PMID23715995
PMCPMC4476508
OpenAlexW1978539060

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.