Evidence map›Paper›PMID 18044683›Full record

ReviewInternational journal of chronic obstructive pulmonary disease2007

Genetic predisposition to accelerated decline of lung function in COPD.

Néstor A Molfino

Open access · greenAbstract readReview
In one paragraph

Review in International journal of chronic obstructive pulmonary disease, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. A Systematic Literature Review of the Humanistic Burden of COPD.International journal of chronic obstructive pulmonary disease
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Lung function in our aging population.European journal of medical research · 2011
    Article
  10. Time for new reference values for ventilatory lung function.European journal of medical research · 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

1 author at 1 institution in 1 country.

Néstor A MolfinoOtsuka Maryland Research Institute, Rockville, MD 20850, USA. nestorm@otsuka.com
Otsuka (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Environmental exposures and genetic susceptibility can contribute to lung function decline in chronic obstructive pulmonary disease (COPD). The environmental factors are better known than the genetic factors. One of the commonest reasons of accelerated forced expiratory volume in one second (FEV1) decline in COPD is the continuation of the smoking habit. In addition, COPD patients have frequent acute respiratory infections which can also accelerate the decline of FEV1. All of the gene variants that have been reported in association with accelerated decline of lung function in COPD represent advancement because the findings generate plausible hypotheses about the possible mechanisms by which gene products could accelerate or avert FEV1 decline. Unfortunately, the results have not been consistently replicated and, animal models required to functionally assess the genetic findings, have not yet yielded sufficient data. Genome-wide association studies should provide more definitive results in COPD and other multigenic conditions. Until these studies are reported, the data to date suggest that products encoded by the alpha-1 antitrypsin, some matrix metalloproteinases, and a number of antioxidant genes are associated with accelerated FEV1 decline in COPD. Data on gene variants associated with acute exacerbations of COPD are now emerging.

Indexed as

alpha 1-AntitrypsinAnimalsAntioxidantsDisease ProgressionForced Expiratory VolumeGenetic Predisposition to DiseaseHumansLungMatrix MetalloproteinasesPulmonary Disease, Chronic ObstructiveRespiratory Tract InfectionsRisk FactorsSmokingalpha 1-AntitrypsinAntioxidantsMatrix Metalloproteinases

Identifiers

PMID18044683
PMCPMC2695610
OpenAlexW1481228586

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.