Evidence map›Paper›PMID 34848800›Full record

ArticleScientific reports2021

The strong correlation between ADAM33 expression and airway inflammation in chronic obstructive pulmonary disease and candidate for biomarker and treatment of COPD.

Muhammad Fachri, Mochammad Hatta, Muhammad Nasrum Massi, Arif Santoso, Tri Ariguntar Wikanningtyas, Ressy Dwiyanti, Ade Rifka Junita, Muhammad Reza Primaguna, Muhammad Sabir

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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  13. Review
  14. Article
  15. IL-17A Promotes Epithelial ADAM9 Expression in Cigarette Smoke-Related COPD.International journal of chronic obstructive pulmonary disease · 2022
    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

9 authors at 3 institutions in 1 country.

Muhammad FachriDepartment of Pulmonology and Respiratory Medicine, Faculty of Medicine and Health, Universitas Muhammadiyah, Jakarta, Indonesia.ORCID 0000-0002-4429-822X
Mochammad HattaMolecular Biology and Immunology Laboratory, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia. hattaram@yahoo.com.ORCID 0000-0002-8456-4203
Muhammad Nasrum MassiMolecular Biology and Immunology Laboratory, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia.
Arif SantosoDepartment of Pulmonology and Respiratory Medicine, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia.
Tri Ariguntar WikanningtyasDepartment of Clinical Pathology, Faculty of Medicine and Health, Universitas Muhammadiyah, Jakarta, Indonesia.
Ressy DwiyantiMolecular Biology and Immunology Laboratory, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia.
Ade Rifka JunitaMolecular Biology and Immunology Laboratory, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia.
Muhammad Reza PrimagunaDepartment of Internal Medicine, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia.
Muhammad SabirDepartment of Medical Microbiology, Faculty of Medicine, Tadulako University, Palu, Indonesia.
Hasanuddin University · IDTadulako University · IDUniversitas Muhammadiyah Jakarta · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway inflammation in patients with chronic obstructive pulmonary disease (COPD) is an amplified response of the normal immune system that occurs as a result of chronic irritation by toxic substances, such as cigarette smoke. This leads to the characteristic pathological changes in the inflammatory cells of COPD patients. ADAM33 has been reported to be involved in the pathogenesis of COPD in East Asia by affecting airway inflammation and other immune responses. The aim of this study was to determine the potential role of ADAM33 (mRNA and soluble levels) as a biomarker of inflammation in COPD patients. This is a case control study using consecutive sampling. The COPD case and control (non-COPD) groups comprised 37 and 29 patients, respectively. We used univariate analysis to assess differences in the parameters between the groups and bivariate analysis to non-parametrically compare these parameters between the two groups. We observed significantly higher mRNA levels of ADAM33 in the COPD patients (10.39 ± 1.76) as compared to that in the non-COPD individuals (6.93 ± 0.39; P < 0.001). The levels of soluble ADAM33 were also significantly higher in the COPD patients (2.188 ± 1.142 ng/ml) compared to the non-COPD individuals (0.487 ± 0.105 ng/ml; P < 0.001). The mRNA and soluble ADAM33 levels were significantly higher in COPD patients compared to those in the parameter-matched non-COPD individuals. Thus, ADAM33 is a potential biomarker and treatment for inflammation in COPD patients.

Indexed as

Gene Expression RegulationADAM ProteinsAgedAged, 80 and overBiomarkersCase-Control StudiesFemaleHumansInflammationLinear ModelsLungMaleMiddle AgedPolymorphism, Single NucleotidePulmonary Disease, Chronic ObstructiveRespiratory SystemADAM33 protein, humanADAM ProteinsBiomarkersRNA, MessengerSmoke

Identifiers

PMID34848800
PMCPMC8632976
OpenAlexW3175879939

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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.