Evidence map›Paper›PMID 42625593›Full record

ArticleFrontiers in pharmacology2026

PM2.5 induces lung injury via mtDNA-cGAS-STING-mediated macrophage M1 polarization.

Bingbing Yan, Bomiao Qing, Manling Jiang, Qin Ran, Anying Xiong, Xiang He, Junyi Wang, Lei Zhang, Keyue Wang, Xiaolan Li and 1 more

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Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Bingbing Yan *Clinical Medicine Department, North Sichuan Medical College, Nanchong, China.
Bomiao QingLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Manling JiangLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Qin RanLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Anying XiongLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Xiang HeLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Junyi WangLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Lei ZhangLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Keyue WangLaboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Xiaolan Li *Laboratory of Allergy and Precision Medicine, Chengdu Institute of Respiratory Health, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Guoping LiClinical Medicine Department, North Sichuan Medical College, Nanchong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Exposure to fine particulate matter (PM2.5) is a well-established risk factor for lung inflammation and injury. Macrophages are key innate immune cells in the lung and play critical roles in maintaining pulmonary immune homeostasis and orchestrating inflammatory responses following environmental insults. However, the precise mechanisms by which PM2.5 modulates macrophage function and contributes to lung injury remain incompletely understood. This study aimed to investigate the role of macrophage phenotypic polarization in PM2.5-induced lung injury and the underlying molecular mechanisms. Methods: A subacute exposure (21-day) PM2.5 mouse model and bone marrow-derived macrophages (BMDMs) were used Results: PM2.5 exposure triggered pulmonary inflammation and tissue injury, accompanied by increased pulmonary macrophage accumulation and polarization toward the pro-inflammatory M1 phenotype. Mechanistically, PM2.5 induced mitochondrial damage in macrophages, leading to mtDNA release and subsequent activation of cGAS-STING signaling. Pharmacological inhibition of cGAS with RU.521 attenuated STING pathway activation, macrophage M1 polarization, and PM2.5-induced pulmonary inflammation and lung injury in mice. Conclusions: Our study indicates that PM2.5 promotes lung injury by driving macrophage M1 polarization through an mtDNA-cGAS-STING axis, highlighting cGAS-STING signaling as a potential therapeutic target for PM2.5-related lung injury.

Indexed as

cGAS-STINGlung injurymacrophage polarizationmtDNAPM2.5

Identifiers

PMID42625593
PMCPMC13489883

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