Evidence map›Paper›PMID 22291954›Full record

ArticlePloS one2012

Association between variations in cell cycle genes and idiopathic pulmonary fibrosis.

Nicoline M Korthagen, Coline H M van Moorsel, Nicole P Barlo, Karin M Kazemier, Henk J T Ruven, Jan C Grutters

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

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  18. p53: A Key Protein That Regulates Pulmonary Fibrosis.Oxidative medicine and cellular longevity · 2020
    Review
  19. The genetics of interstitial lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2019
    Review
  20. 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

6 authors at 2 institutions in 1 country.

Nicoline M KorthagenCenter of Interstitial Lung Diseases, St Antonius Hospital, Nieuwegein, The Netherlands.
Coline H M van Moorsel
Nicole P Barlo
Karin M Kazemier
Henk J T Ruven
Jan C Grutters
St. Antonius Ziekenhuis · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a devastating and progressive lung disease. Its aetiology is thought to involve damage to the epithelium and abnormal repair. Alveolar epithelial cells near areas of remodelling show an increased expression of proapoptotic molecules. Therefore, we investigated the role of genes involved in cell cycle control in IPF. Genotypes for five single nucleotide polymorphisms (SNPs) in the tumour protein 53 (TP53) gene and four SNPs in cyclin-dependent kinase inhibitor 1A (CDKN1A), the gene encoding p21, were determined in 77 IPF patients and 353 controls. In peripheral blood mononuclear cells (PBMC) from 16 healthy controls mRNA expression of TP53 and CDKN1A was determined. Rs12951053 and rs12602273, in TP53, were significantly associated with survival in IPF patients. Carriers of a minor allele had a 4-year survival of 22% versus 57% in the non-carrier group (p = 0.006). Rs2395655 and rs733590, in CDKN1A, were associated with an increased risk of developing IPF. In addition, the rs2395655 G allele correlated with progression of the disease as it increased the risk of a rapid decline in lung function. Functional experiments showed that rs733590 correlated significantly with CDKN1A mRNA expression levels in healthy controls. This is the first study to show that genetic variations in the cell cycle genes encoding p53 and p21 are associated with IPF disease development and progression. These findings support the idea that cell cycle control plays a role in the pathology of IPF. Variations in TP53 and CDKN1A can impair the response to cell damage and increase the loss of alveolar epithelial cells.

Indexed as

AgedCase-Control StudiesCyclin-Dependent Kinase Inhibitor p21FemaleGene FrequencyGenes, cdcGenes, p53Genetic Association StudiesGenetic Predisposition to DiseaseHumansIdiopathic Pulmonary FibrosisLinkage DisequilibriumMaleMiddle AgedPolymorphism, Single NucleotideSurvival AnalysisCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21

Identifiers

PMID22291954
PMCPMC3264581
OpenAlexW1971738121

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.