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Peer-reviewedCC BY-NC-NDRespiratory research

Pirfenidone reduces fine particulate matter-induced epithelial to mesenchymal transition in lung epithelial cells through regulating mitochondrial fission and autophagy.

  • Yu-Chen Chen1,2
  • Ya-Chun Chen1
  • Wei Chang1
  • I-Ta Lee3
  • Wen-Zhuang Then1,4
  • Yu-Chi Chiu5,6
  • Chiang-Wen Lee7
  • Tzu-Yi Chuang8
  • Yuh-Lien Chen9
9 affiliations
  1. 1Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, No. 1, Sec 1, Ren-Ai Road, Taipei, Taiwan ROC.
  2. 2Department of Medicine, Mackay Medical College, New Taipei City, Taiwan.
  3. 3School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
  4. 4Department of Cardiovascular Surgery, Lo-Hsu Medical Foundation, Lotung Poh-Ai Hospital, Yilan, Taiwan.
  5. 5Department of Pulmonary Medicine, Taoyuan General Hospital, Ministry of Health and Welfare, No.1492, Zhongshan Rd., Taoyuan Dist., Taoyuan, 330, Taiwan ROC.
  6. 6Department of Nursing, Yuanpei University of Medical Technology, Hsinchu, Taiwan.
  7. 7Department of Respiratory Care and Chronic Diseases and Health Promotion Research Center, Chang Gung University of Science and Technology, No. 2, West Section of Jiapu Road, Puzi City, Chiayi County, 613, Taiwan ROC. [email protected].
  8. 8Department of Pulmonary Medicine, Taoyuan General Hospital, Ministry of Health and Welfare, No.1492, Zhongshan Rd., Taoyuan Dist., Taoyuan, 330, Taiwan ROC. [email protected].
  9. 9Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, No. 1, Sec 1, Ren-Ai Road, Taipei, Taiwan ROC. [email protected].
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Abstract

Background

Epidemiological studies have shown that fine particulate matter (PM) is closely associated with increased morbidity and mortality from lung diseases. However, the mechanisms by which PM affects alveolar epithelial-mesenchymal transition (EMT), such as mitochondrial dysfunction, remain unclear, and therapy options require further investigation.Methods

Human type II alveolar epithelial cells (A549 cells) were exposed to 100 µg/mL PM to investigate EMT induction. In an animal model, mice were exposed to PM via intratracheal injection to simulate air pollution exposure.Results

PM exposure reduced the expression of the epithelial marker E-cadherin while increasing the expression of mesenchymal markers vimentin, α-smooth muscle actin (α-SMA), and transforming growth factor β1 (TGF-β1). Furthermore, the expression of EMT-related transcription factors Snail and Slug was upregulated, accompanied by a morphological shift in A549 cells from cubic to spindle shapes and enhanced cell migration. PM also promoted mitochondrial fission and induced the accumulation of LC3B and p62 proteins. Treatment with the antifibrotic drug pirfenidone (PFD) effectively reduced PM-induced EMT-related protein expression and cell migration. These effects are achieved by reducing mitochondrial fission, increasing autophagosome accumulation, and related autophagic degradation. The lungs of PM-treated mice showed increased expression of EMT-related proteins, significant blood cell infiltration, and alveolar wall thickening. PFD treatment significantly improved these conditions and reduced collagen deposition.Conclusion

PM induces increased mitochondrial fission and incomplete autophagy (characterized by autophagosome accumulation and impaired flux), leading to EMT. PFD treatment can also effectively reduce PM-induced EMT formation by modulating these pathways.

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Cite

BibTeXRIS
BibTeX
@article{chen2026pirfenidone,
  title = {{Pirfenidone reduces fine particulate matter-induced epithelial to mesenchymal transition in lung epithelial cells through regulating mitochondrial fission and autophagy.}},
  author = {Yu-Chen Chen and Ya-Chun Chen and Wei Chang and I-Ta Lee and Wen-Zhuang Then and Yu-Chi Chiu and Chiang-Wen Lee and Tzu-Yi Chuang and Yuh-Lien Chen},
  journal = {Respiratory research},
  year = {2026},
  month = aug,
  doi = {10.1186/s12931-026-03804-1},
  url = {https://europepmc.org/article/MED/42958371},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Pirfenidone reduces fine particulate matter-induced epithelial to mesenchymal transition in lung epithelial cells through regulating mitochondrial fission and autophagy.
AU  - Yu-Chen Chen
AU  - Ya-Chun Chen
AU  - Wei Chang
AU  - I-Ta Lee
AU  - Wen-Zhuang Then
AU  - Yu-Chi Chiu
AU  - Chiang-Wen Lee
AU  - Tzu-Yi Chuang
AU  - Yuh-Lien Chen
PY  - 2026
DA  - 2026/08/01
JO  - Respiratory research
DO  - 10.1186/s12931-026-03804-1
UR  - https://europepmc.org/article/MED/42958371
AB  - Background  Epidemiological studies have shown that fine particulate matter (PM) is closely associated with increased morbidity and mortality from lung diseases. However, the mechanisms by which PM affects alveolar epithelial-mesenchymal transition (EMT), such as mitochondrial dysfunction, remain unclear, and therapy options require further investigation.Methods  Human type II alveolar epithelial cells (A549 cells) were exposed to 100 µg/mL PM to investigate EMT induction. In an animal model, mice were exposed to PM via intratracheal injection to simulate air pollution exposure.Results  PM exposure reduced the expression of the epithelial marker E-cadherin while increasing the expression of mesenchymal markers vimentin, α-smooth muscle actin (α-SMA), and transforming growth factor β1 (TGF-β1). Furthermore, the expression of EMT-related transcription factors Snail and Slug was upregulated, accompanied by a morphological shift in A549 cells from cubic to spindle shapes and enhanced cell migration. PM also promoted mitochondrial fission and induced the accumulation of LC3B and p62 proteins. Treatment with the antifibrotic drug pirfenidone (PFD) effectively reduced PM-induced EMT-related protein expression and cell migration. These effects are achieved by reducing mitochondrial fission, increasing autophagosome accumulation, and related autophagic degradation. The lungs of PM-treated mice showed increased expression of EMT-related proteins, significant blood cell infiltration, and alveolar wall thickening. PFD treatment significantly improved these conditions and reduced collagen deposition.Conclusion  PM induces increased mitochondrial fission and incomplete autophagy (characterized by autophagosome accumulation and impaired flux), leading to EMT. PFD treatment can also effectively reduce PM-induced EMT formation by modulating these pathways.
SN  - 1465-9921
SN  - 1465-993X
ER  -