Evidence map›Paper›PMID 41864062›Full record

ArticleEBioMedicine2026

PPAR-γ suppresses macrophage senescence and allergic airway inflammation through controlling lipid metabolic pathways.

Wenjing Gu, Rongjun Wan, Zhifeng Chen, Wenshen Wang, Shaobing Xie, Chuangli Hao, Guangshu Liu, Mei Wan, Peisong Gao

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases.Journal of respiratory biology and translational medicine · 2026
    Article
  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Wenjing GuDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Respiratory Medicine, Children's hospital of Soochow University, Suzhou, Jiangsu, China.
Rongjun WanDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Wannan Medical College, Wuhu, Anhui, China.
Zhifeng ChenDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Respiratory Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Wenshen WangDepartment of Radiology & Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Shaobing XieDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Chuangli HaoDepartment of Respiratory Medicine, Children's hospital of Soochow University, Suzhou, Jiangsu, China.
Guangshu LiuDepartment of Radiology & Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Mei WanDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Peisong GaoDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: pgao1@jhmi.edu.

Funding

Environmental Pollutants Potentiate Allergic Inflammation via Functional Axis of Aryl hydrocarbon Receptor, ROS, and CaMKII in AsthmaR01AI141642 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2019 to 2024
$2.9M
Functional role of miR-511-3p in allergic asthma and its underlying mechanismsR01AI153331 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Peisong Gao · 2021 to 2026
$2.7M
NIAID NIH HHS R01 AI141642NIAID NIH HHS R01 AI153331
6 · The paper itself

Abstract

backgroundCellular senescence has emerged as a key contributor to the pathogenesis of chronic lung diseases. Peroxisome proliferator-activated receptor gamma (PPAR-γ), a nuclear transcription factor, regulates senescence across multiple cell types. However, the role of PPAR-γ in allergic airway inflammation, particularly through regulation of macrophage senescence, remains poorly defined.

methodsCellular senescence was evaluated in an allergic asthma mouse model using single-cell RNA sequencing (scRNA-seq). Senescent cells were selectively eliminated with dasatinib and quercetin (D&Q) to assess their contribution to disease pathogenesis. Macrophage-lineage-specific PPAR-γ conditional knockout model (Pparg

findingsscRNA-seq analysis revealed enhanced senescence signatures in mononuclear phagocytes (MNPs), characterised by increased SenMayo scores and elevated Cdkn2a (p16) expression. Clearance of senescent cells significantly reduced airway inflammation and Th2 cytokine levels (IL-4, IL-5). Correlation analysis identified PPAR-γ as a key transcriptional regulator inversely associated with cellular senescence. Macrophage-lineage-specific deletion of PPAR-γ (Pparg

interpretationThese findings identify macrophage senescence as a pathogenic driver of allergic airway inflammation and establish PPAR-γ as a critical regulator of macrophage senescence and homoeostasis, highlighting its potential as a therapeutic target for asthma.

fundingUS National Institutes of Health (NIH) (1R01AI153331 and R01AI141642 to Dr. Gao), Anhui Provincial Key projects of Natural Science Foundation for Colleges and Universities 2025AHGXZK31476 (Dr. Wan).

Indexed as

AsthmaCellular SenescenceLipid MetabolismMacrophagesPPAR gammaAnimalsCytokinesDisease Models, AnimalInflammationMacrophages, AlveolarMiceMice, KnockoutPPAR-gamma AgonistsCytokinesPPAR gammaPPAR-gamma AgonistsAsthmaCellular senescenceLipid metabolismLiposomeMacrophagePPAR-γRosiglitazone

Identifiers

PMID41864062
PMCPMC13018883

What OpenQuestion holds

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LicenceCC BY
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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.