Evidence map›Paper›PMID 42631787›Full record

ReviewMolecular diagnosis & therapy2026

Integrative Omics of Eosinophils in Asthma and COPD: Deciphering Molecular Signatures for Targeted Therapy.

Jun Miyata, Keeya Sunata, Hisashi Sasaki, Shotaro Chubachi, Yoshinori Hasegawa, Yusuke Kawashima, Makoto Arita, Koichi Fukunaga

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular diagnosis & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Jun MiyataDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan. junmiyata.a2@keio.jp.ORCID http://orcid.org/0000-0002-3189-1702
Keeya SunataDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.ORCID http://orcid.org/0000-0002-1694-8432
Hisashi SasakiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.ORCID http://orcid.org/0000-0001-7642-2451
Shotaro ChubachiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.ORCID http://orcid.org/0000-0002-5046-3762
Yoshinori HasegawaDepartment of Applied Genomics, Kazusa DNA Research Institute, Chiba, Japan.ORCID http://orcid.org/0000-0003-2904-6611
Yusuke KawashimaDepartment of Applied Genomics, Kazusa DNA Research Institute, Chiba, Japan.ORCID http://orcid.org/0000-0002-9779-8199
Makoto AritaLaboratory for Metabolomics, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan.ORCID http://orcid.org/0000-0001-9902-0463
Koichi FukunagaDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.ORCID http://orcid.org/0000-0001-7460-1990

Funding

Japan Agency for Medical Research and Development 22ek0410097Japan Agency for Medical Research and Development 25ek0410138Japan Society for the Promotion of Science 20K17239Japan Society for the Promotion of Science 24K11605
6 · The paper itself

Abstract

Eosinophils are central effector and regulatory cells in asthma and eosinophilic respiratory disease, and a clinically relevant subset in a proportion of patients with chronic obstructive pulmonary disease (COPD) and asthma-COPD overlap. While eosinophil counts are established biomarkers to guide corticosteroid and biologic therapy, they do not capture the molecular heterogeneity of eosinophil activation across these conditions. Advances in integrative omics now permit comprehensive profiling of eosinophils at the transcriptomic, proteomic, and lipidomic levels. In this narrative review we summarize eosinophil-focused single-omics and multi-omics studies in asthma and COPD, with an emphasis on severe eosinophilic asthma and eosinophilic COPD. Multi-omics analysis of blood eosinophils in severe asthma has revealed IL-5-dominated pathways that coexist with IL-4 and microbe-responsive programs. In contrast, eosinophils in asthma-COPD overlap and eosinophilic COPD exhibit prominent interferon-γ, tumor necrosis factor-α, and IL-33 signatures. Mechanistic studies further demonstrate that IL-4/IL-13 enhances eosinophil responsiveness to IL-33 and that IL-33 induces extracellular trap formation (ETosis). We discuss how these disease- and context-specific molecular programs may refine biomarker interpretation and inform the rational selection of biologics targeting IL-5/IL-5R, IL-4Rα, TSLP, and IL-33/ST2 in asthma and COPD.

Identifiers

What Socratic holds

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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 Socratic graph.