Evidence map›Paper›PMID 37592330›Full record

ArticleRespiratory research2023

Apoptosis inhibitor of macrophage (AIM)/CD5L is involved in the pathogenesis of COPD.

Michiko Takimoto-Sato, Masaru Suzuki, Hiroki Kimura, Haiyan Ge, Munehiro Matsumoto, Hironi Makita, Satoko Arai, Toru Miyazaki, Masaharu Nishimura, Satoshi Konno

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed, 11 citations in OpenAlex.

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  6. Cigarette Smoking and Atherosclerotic Cardiovascular Disease.Journal of atherosclerosis and thrombosis · 2024
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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

10 authors at 5 institutions in 3 countries.

Michiko Takimoto-SatoDepartment of Respiratory Medicine, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-ku, Sapporo, 060-8638, Japan.
Masaru SuzukiDepartment of Respiratory Medicine, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-ku, Sapporo, 060-8638, Japan. suzumasa@med.hokudai.ac.jp.
Hiroki KimuraDepartment of Respiratory Medicine, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-ku, Sapporo, 060-8638, Japan.
Haiyan GeDepartment of Respiratory and Critical Care Medicine, Huadong Hospital, Fudan University, Shanghai, China.
Munehiro MatsumotoDepartment of Respiratory Medicine, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-ku, Sapporo, 060-8638, Japan.
Hironi MakitaHokkaido Medical Research Institute of Respiratory Diseases, Sapporo, Japan.
Satoko AraiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Toru MiyazakiThe Institute for AIM Medicine, Tokyo, Japan.
Masaharu NishimuraDepartment of Respiratory Medicine, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-ku, Sapporo, 060-8638, Japan.
Satoshi KonnoDepartment of Respiratory Medicine, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-ku, Sapporo, 060-8638, Japan.
Hokkaido University · JPHokkaido Institute of Public Health · JPFudan University · CNJapan Agency for Medical Research and Development · JPThe University of Tokyo · JP

Funding

AMED-LEAP JP22gm0010006h
6 · The paper itself

Abstract

backgroundAlveolar macrophages (AMs) and AM-produced matrix metalloprotease (MMP)-12 are known to play critical roles in the pathogenesis of chronic obstructive pulmonary disease (COPD). The apoptosis inhibitor of the macrophages (AIM)/CD5 molecule-like (CD5L) is a multifunctional protein secreted by the macrophages that mainly exists in the blood in a combined form with the immunoglobulin (Ig)M pentamer. Although AIM has both facilitative and suppressive roles in various diseases, its role in COPD remains unclear.

methodsWe investigated the role of AIM in COPD pathogenesis using porcine pancreas elastase (PPE)-induced and cigarette smoke-induced emphysema mouse models and an in vitro model using AMs. We also analyzed the differences in the blood AIM/IgM ratio among nonsmokers, healthy smokers, and patients with COPD and investigated the association between the blood AIM/IgM ratio and COPD exacerbations and mortality in patients with COPD.

resultsEmphysema formation, inflammation, and cell death in the lungs were attenuated in AIM

conclusionsAIM facilitates the development of COPD by upregulating MMP-12. Additionally, a higher blood AIM/IgM ratio was associated with poor prognosis in patients with COPD.

trial registrationThis clinical study, which included nonsmokers, healthy smokers, and smokers with COPD, was approved by the Ethics Committee of the Hokkaido University Hospital (012-0075, date of registration: September 5, 2012). The Hokkaido COPD cohort study was approved by the Ethics Committee of the Hokkaido University School of Medicine (med02-001, date of registration: December 25, 2002).

Indexed as

Apoptosis Regulatory ProteinsEmphysemaPulmonary Disease, Chronic ObstructivePulmonary EmphysemaAnimalsApoptosisCohort StudiesHumansImmunoglobulin MMacrophagesMatrix Metalloproteinase 12MiceReceptors, ScavengerApoptosis Regulatory ProteinsCD5L protein, humanCd5l protein, mouseImmunoglobulin MMatrix Metalloproteinase 12Receptors, ScavengerAlveolar macrophageApoptosis inhibitor of macrophageChronic obstructive lung diseaseMatrix metalloprotease-12

Identifiers

PMID37592330
PMCPMC10433671
OpenAlexW4385951317

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Registered trials

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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.