Evidence map›Paper›PMID 18508830›Full record

ArticleThe European respiratory journal2008

Angiotensinogen gene G-6A polymorphism influences idiopathic pulmonary fibrosis disease progression.

M Molina-Molina, A Xaubet, X Li, A Abdul-Hafez, K Friderici, K Jernigan, W Fu, Q Ding, J Pereda, A Serrano-Mollar and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The European respiratory journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

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  10. Review
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  12. Article
  13. Angiotensinogen gene transcription in pulmonary fibrosis.International journal of peptides · 2012
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. JunD and HIF-1alpha mediate transcriptional activation of angiotensinogen by TGF-beta1 in human lung fibroblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009
    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

16 authors at 6 institutions in 2 countries.

M Molina-MolinaServicio de Neumología, Hospital Clínic, Instituto de Investigaciones Biomédicas Agusti Pi Suñer, Barcelona, Spain. mariamolinamolina@hotmail.com
A Xaubet
X Li
A Abdul-Hafez
K Friderici
K Jernigan
W Fu
Q Ding
J Pereda
A Serrano-Mollar
A Casanova
E Rodríguez-Becerra
F Morell
J Ancochea
C Picado
B D Uhal
Centro de Investigación Biomédica en Red · ESMichigan State University · USHospital Universitario de La Princesa · ESCancer Research And Biostatistics · USHospital Clínic de Barcelona · ESHospital Universitario Virgen del Rocío · ES

Funding

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

Abstract

Angiotensin II is a growth factor that plays a key role in the physiopathology of idiopathic pulmonary fibrosis (IPF). A nucleotide substitution of an adenine instead of a guanine (G-6A) in the proximal promoter region of angiotensinogen (AGT), the precursor of angiotensin II, has been associated with an increased gene transcription rate. In order to investigate whether the G-6A polymorphism of the AGT gene is associated with IPF development, severity and progression, the present study utilised a case-control study design and genotyped G-6A in 219 patients with IPF and 224 control subjects. The distribution of G-6A genotypes and alleles did not significantly differ between cases and controls. The G-6A polymorphism of the AGT gene was not associated with disease severity at diagnosis. The presence of the A allele was strongly associated with increased alveolar arterial oxygen tension difference during follow-up, after controlling for the confounding factors. Higher alveolar arterial oxygen tension changes over time were observed in patients with the AA genotype (0.37+/-0.7 mmHg (0.049+/-0.093 kPa) per month) compared to GA genotype (0.12+/-1 mmHg (0.016+/-0.133 kPa) per month) and GG genotype (0.2+/-0.6 mmHg (0.027+/-0.080 kPa) per month). G-6A polymorphism of the angiotensinogen gene is associated with idiopathic pulmonary fibrosis progression but not with disease predisposition. This polymorphism could have a predictive significance in idiopathic pulmonary fibrosis patients.

Indexed as

Polymorphism, GeneticAdultAgedAllelesAngiotensinogenDisease ProgressionFemaleGenotypeGuanineHumansIdiopathic Pulmonary FibrosisMaleMiddle AgedPromoter Regions, GeneticPulmonary Gas ExchangeAngiotensinogenGuanine

Identifiers

PMID18508830
PMCPMC3255086
OpenAlexW2141148779

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.