ArticleJournal of thoracic disease2023
PM2.5 induces lung inflammation and fibrosis via airway smooth muscle cell expression of the Wnt5a/JNK pathway.
Article in Journal of thoracic disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- The miR-155-5p/SOCS1/NF-κB Axis Regulates Airway Smooth Muscle Dysfunction and is a Potential Therapeutic Candidate of Chronic Obstructive Pulmonary Disease.Inflammation · 2026Article
- Health Risk and Pathogenesis of PMToxics · 2026Review
- Effective-Component Compatibility of Bufei Yishen Formula III Improves Chronic Obstructive Pulmonary Disease by Inhibiting Inflammatory Responses Through Blocking PTX3 Activation.Journal of inflammation research · 2026Article
- Long-term and short-term exposure to outdoor air pollution and its association with glycolipid metabolic disorders.World journal of diabetes · 2025Article
- The role of neutrophils in bronchiectasis.Annals of medicine · 2025Review
- Article
- Respiratory health and chronic disease risks in residents of agricultural areas in Chiang Mai, Northern Thailand.PloS one · 2025Article
- Bone Marrow Mesenchymal Stem Cells-Derived Exosomes Inhibit Apoptosis of Pulmonary Microvascular Endothelial Cells in COPD Mice Through miR-30b/Wnt5a Pathway.International journal of nanomedicine · 2025Article
- Epigenetic Inhibitors Differentially Impact TGF-β1 Signaling Cascades in COPD Airway Smooth Muscle Cells.Cells · 2024Article
- Downregulation of tRNA methyltransferase FTSJ1 by PM2.5 promotes glycolysis and malignancy of NSCLC via facilitating PGK1 expression and translation.Cell death & disease · 2024Article
- TRPV4 Activation during Guinea Pig Airway Smooth Muscle Contraction Promotes CaPharmaceuticals (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: In recent years, particulate matter 2.5 (PM2.5) exposure has been considered a key dangerous factor in chronic obstructive pulmonary disease (COPD). The dysfunction of airway smooth muscle cells (ASMCs) facilitates lung inflammation and fibrosis in COPD. Therefore, we explored whether PM2.5 could promote the inflammatory response and fibrosis in ASMCs Methods: Wnt5a expression in the bronchoalveolar lavage fluid (BALF) of COPD patients exposed to PM2.5 was measured by enzyme-linked immunosorbent assay (ELISA). Mice were intratracheally injected with PM2.5 and a Wnt5a antagonist (BOX5). ASMCs were transfected with Results: We found that the increase in Wnt5a expression in the BALF of COPD patients was positively correlated with the levels of PM2.5 exposure. The Wnt5a/JNK/NF-κB pathway was activated in the lung samples of PM2.5-induced model mice and PM2.5-exposed ASMCs, which promoted the production of α-SMA, collagen I and collagen III and increased the secretion of IL-6, IL-8 and TNF-α. Furthermore, our results showed that BOX5 could prevent these effects. Conclusions: These findings suggest that PM2.5 stimulation of ASMCs induces pulmonary inflammatory factor expression and collagen deposition during COPD via the Wnt5a/JNK pathway, which indicates that modulating the Wnt5a/JNK pathway could be a promising therapeutic strategy for PM2.5-induced COPD.
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