Evidence map›Paper›PMID 39153120›Full record

ArticleLung2024

Adam19 Deficiency Impacts Pulmonary Function: Human GWAS Follow-up in a Mouse Knockout Model.

Huiling Li, John S House, Cody E Nichols, Artiom Gruzdev, James M Ward, Jian-Liang Li, Annah B Wyss, Ezazul Haque, Matthew L Edin, Susan A Elmore and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Lung, 2024. 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
–field-weighted citation impact
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.

  1. Preclinical models of COPD: a state of the art review.The European respiratory journal · 2026
    Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Huiling LiImmunity, Inflammation and Disease Laboratory, Division of Intramural Research, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, MD A3-05, PO Box 12233, Research Triangle Park, North Carolina, 27709, USA.
John S HouseBiostatistics & Computational Biology Branch, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Cody E NicholsWhitsell Innovations, Inc., Chapel Hill, North Carolina, USA.
Artiom GruzdevReproductive & Developmental Biology Laboratory, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
James M WardIntegrative Bioinformatics Support Group, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Jian-Liang LiIntegrative Bioinformatics Support Group, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Annah B WyssCardiovascular Institute, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Ezazul HaqueImmunity, Inflammation and Disease Laboratory, Division of Intramural Research, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, MD A3-05, PO Box 12233, Research Triangle Park, North Carolina, 27709, USA.
Matthew L EdinImmunity, Inflammation and Disease Laboratory, Division of Intramural Research, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, MD A3-05, PO Box 12233, Research Triangle Park, North Carolina, 27709, USA.
Susan A ElmoreCellular & Molecular Pathology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Beth W MahlerCellular & Molecular Pathology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Laura M DegraffImmunity, Inflammation and Disease Laboratory, Division of Intramural Research, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, MD A3-05, PO Box 12233, Research Triangle Park, North Carolina, 27709, USA.
Min ShiBiostatistics & Computational Biology Branch, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Darryl C ZeldinImmunity, Inflammation and Disease Laboratory, Division of Intramural Research, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, MD A3-05, PO Box 12233, Research Triangle Park, North Carolina, 27709, USA.
Stephanie J LondonImmunity, Inflammation and Disease Laboratory, Division of Intramural Research, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, MD A3-05, PO Box 12233, Research Triangle Park, North Carolina, 27709, USA. london2@niehs.nih.gov.

Funding

Genetic Analyses For Epidemiologic Studies Of Respiratory DiseaseZIAES025045 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI LONDON, STEPHANIE · 2009 to 2025
$7.3M
INDOOR ALLERGENS AND ASTHMAZ01ES025041 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ZELDIN, DARRYL C · 1998 to 2008
$1.9M
Genetic /Environment Factors In Nonmalignant Resp DisZ01ES043012 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI LONDON, STEPHANIE JOAN · 1999 to 2008
$340k
Genetic Analyses For Epidemioloy Of Respiratory DiseaseZ01ES025045 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI LONDON, STEPHANIE JOAN · 2000 to 2008
$238k
Intramural NIH HHS Z01 ES025041Intramural NIH HHS Z01 ES025045Intramural NIH HHS Z01 ES043012Intramural Research Program of the NIH and NIEHS Z01 ES 025041Intramural Research Program of the NIH and NIEHS Z01 ES025045 and Z01 ES043012
6 · The paper itself

Abstract

purposeOver 550 loci have been associated with human pulmonary function in genome-wide association studies (GWAS); however, the causal role of most remains uncertain. Single nucleotide polymorphisms in a disintegrin and metalloprotease domain 19 (ADAM19) are consistently related to pulmonary function in GWAS. Thus, we used a mouse model to investigate the causal link between Adam19 and pulmonary function.

methodsWe created an Adam19 knockout (KO) mouse model and validated the gene targeting using RNA-Seq and RT-qPCR. Mouse body composition was assessed using dual-energy X-ray absorptiometry. Mouse lung function was measured using flexiVent.

resultsContrary to prior publications, the KO was not neonatal lethal. KO mice had lower body weight and shorter tibial length than wild-type (WT) mice. Their body composition revealed lower soft weight, fat weight, and bone mineral content. Adam19 KO had decreased baseline respiratory system elastance, minute work of breathing, tissue damping, tissue elastance, and forced expiratory flow at 50% forced vital capacity but higher FEV

conclusionOur murine findings support a causal role of ADAM19, implicated in human GWAS, in regulating pulmonary function.

Indexed as

ADAM ProteinsGenome-Wide Association StudyLungAnimalsBody CompositionDisease Models, AnimalFemaleHumansMaleMiceMice, KnockoutPolymorphism, Single NucleotideRespiratory Function TestsVital CapacityADAM19 protein, humanAdam19 protein, mouseADAM ProteinsFlexiVentInflammationLung functionMeltrin betaRNA-SeqSpirometry

Identifiers

PMID39153120
PMCPMC11427501

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.