ArticleMedicine2017
Genome-wide association study for genetic variants related with maximal voluntary ventilation reveals two novel genomic signals associated with lung function.
Article in Medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Genome-Wide Association Analysis of Rapid Decline in Lung Function: Analysis From the Korean Genome and Epidemiology Study.Journal of Korean medical science · 2024Article
- Maximal Voluntary Ventilation Should Not Be Estimated From the Forced Expiratory Volume in the First Second in Healthy People and COPD Patients.Frontiers in physiology · 2020Article
- Clinical implication of maximal voluntary ventilation in myotonic muscular dystrophy.Medicine · 2019Observational
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) for spirometry parameters have been limited to forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and their ratio. This study examined to identify genetic variants associated with maximal voluntary ventilation (MVV), an important spirometry parameter presenting inspiratory muscle strength.A total of 8842 Korean subjects participated in the Korean Association REsource Consortium were used to identify nucleotide variants associated with MVV and other spirometry parameters through a GWAS. Genetic associations were determined by employing a mixed model that can control background polygenic effects.The analysis revealed 3 nucleotide variants associated with MVV (P < 5 × 10). One (rs1496255) was also associated with FVC and FEV1. The other 2 variants were identified only for MVV and located in the genes of LOC102724340 (rs41434646) and FHIT (rs9833533). In particular, FHIT represses transcriptional activity of β-catenin, a critical protein for growth of skeletal muscle, and thus might have influenced the level of MVV.The current study revealed 2 novel nucleotide variants as genetic association signals for MVV. The association signals were suggested specific for neuromuscular diseases with a restrictive ventilatory impairment. Further studies are required to understand underlying mechanisms for their influence to restrictive lung diseases.
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Registered trials
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