Evidence map›Paper›PMID 41783090›Full record

ArticleMediators of inflammation2026

Circ-Eif3c Carried by M2 Macrophage-Derived Exosomes Mitigates Asthma Progression via miR-15a-5p/GSS/SOCS6 Axis Inhibition.

Jiaying Yuan, Jiayi Zhao, Xiahui Ge, Xingxing Zhu, Li Li, Haoran Ni, Jian Fan, Yi Zhang, Yahong Sun, Yan Shang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Jiaying YuanDepartment of General Practice, Shanghai Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, 200433, China, chhospital.com.cn.
Jiayi ZhaoDepartment of General Practice, Shanghai 411 Hospital, China RongTong Medical Healthcare Group Co., Ltd., Shanghai, 200081, China.ORCID https://orcid.org/0000-0001-9975-9911
Xiahui GeDepartment of Respiratory and Critical Care Medicine, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School Of Medicine, Mohe Road, Shanghai, 201999, China, shsmu.edu.cn.ORCID https://orcid.org/0000-0003-4697-7979
Xingxing ZhuDepartment of Respiratory and Critical Care Medicine, Haining People's Hospital, Haining, 314400, China.
Li LiDepartment of Respiratory and Critical Care Medicine, Shanghai Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, 200433, China, chhospital.com.cn.
Haoran NiDepartment of Respiratory and Critical Care Medicine, Shanghai Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, 200433, China, chhospital.com.cn.
Jian FanDepartment of General Practice, Shanghai Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, 200433, China, chhospital.com.cn.
Yi ZhangDepartment of General Practice, Shanghai Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, 200433, China, chhospital.com.cn.
Yahong SunDepartment of Respiratory and Critical Care Medicine, Haining People's Hospital, Haining, 314400, China.
Yan ShangDepartment of General Practice, Shanghai Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, 200433, China, chhospital.com.cn.ORCID https://orcid.org/0000-0003-2455-1352

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: In the study, we aimed to uncover potential therapeutic mechanisms concerning M2 macrophage-derived exosomes in asthma. Methods: Exosomes were isolated from M0Φ-Exos and M2Φ-Exos. An ovalbumin (OVA)-induced asthma mouse model or lipopolysaccharide (LPS)-induced alveolar epithelial cells (AECs) were created to unravel the therapeutic mechanisms. High-throughput sequencing was used to search for differentially expressed circRNA. Bioinformation analysis and luciferase report analysis were used to reveal the regulationship among circ-Eif3c, miR-15a-5p, glutathione synthetase (GSS), and suppressor of cytokine signaling 6 (SOCS6). Results: The results showed that M2Φ-Exos suppressed OVA-induced inflammatory cytokine secretion and lung injury in mice. Next-generation sequencing (NGS) showed that circ-Eif3c was upregulated in M2Φ-Exos. Circ-Eif3c downregulation inhibited the therapeutic effect of M2Φ-Exos. Bioinformation analysis confirmed that miR-15a-5p, GSS, and SOCS6 were the downstream targets of circ-Eif3c, which were confirmed by luciferase report analysis. The overexpression of miR-15a-5p or the downregulation of GSS/SOCS6 reversed circ-Eif3c's protective effects on LPS-induced AEC damage. The overexpression of circ-Eif3c increased the therapeutic effect of M2Φ-Exos. Conclusion: In conclusion, circ-Eif3c-enriched M2Φ-Exos attenuated airway remodeling by restoring the function of AECs.

Indexed as

AsthmaEukaryotic Initiation Factor-3ExosomesMacrophagesMicroRNAsRNA, CircularSuppressor of Cytokine Signaling ProteinsAnimalsMiceMice, Inbred BALB CEukaryotic Initiation Factor-3MicroRNAsMirn15 microRNA, mouseRNA, CircularSuppressor of Cytokine Signaling Proteinsasthmacirc-Eif3cexosomeM2 macrophagemiR-15a-5p

Identifiers

PMID41783090
PMCPMC12953728

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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.