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Related Experiment Video

Updated: Jun 2, 2026

Forming Micro-and Nano-Plastics from Agricultural Plastic Films for Employment in Fundamental Research Studies
08:21

Forming Micro-and Nano-Plastics from Agricultural Plastic Films for Employment in Fundamental Research Studies

Published on: July 27, 2022

Microplastics as a Cross-Disease Driving Risk Factor in Lung Pathogenesis: An Integrative Study Combining In Silico

Haonan Ruan1, Bufan Zhang1, Qiqi Xu1

  • 1Institute of Medical Genetics and Development, Key Laboratory of Reproductive Genetics (Ministry of Education) and Women's Hospital, Zhejiang University, School of Medicine, Zhejiang, China.

Journal of Applied Toxicology : JAT
|June 1, 2026
PubMed
Summary

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This summary is machine-generated.

Microplastic exposure is linked to lung diseases like COPD, IPF, and LUAD. This study identifies CDK1 as a key target, showing microplastics promote lung fibrosis by upregulating CDK1 in pulmonary fibroblasts.

Area of Science:

  • Environmental toxicology
  • Computational biology
  • Pulmonary medicine

Background:

  • Microplastics (MPs) are emerging environmental pollutants with growing evidence linking them to lung diseases.
  • The precise molecular mechanisms by which MP exposure drives lung disease pathogenesis remain largely unknown.
  • Understanding these mechanisms is crucial for addressing the increasing burden of respiratory illnesses.

Purpose of the Study:

  • To investigate microplastic exposure as a cross-disease risk factor for lung diseases, including COPD, IPF, and LUAD.
  • To identify key molecular targets and pathways involved in MP-induced lung pathogenesis using integrated computational and bioinformatics approaches.
  • To experimentally validate the role of identified targets in MP-driven lung fibrosis.

Main Methods:

Keywords:
computational toxicologycross‐disease driving risk factorlung adenocarcinomalung diseasesmicroplastics

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  • Integrated computational toxicology and bioinformatics analyses to identify shared differentially expressed genes (DEGs) between MP exposure and lung diseases (COPD, IPF, LUAD).
  • Construction and analysis of protein-protein interaction (PPI) networks, followed by enrichment analysis.
  • Validation of key target expression using single-cell datasets and experimental validation in human pulmonary fibroblasts.

Main Results:

  • Identified shared common DEGs (scDEGs) associated with MP exposure and lung diseases, implicating cell cycle, mitosis, and DNA repair pathways.
  • CDK1, BRCA1, and CCND1 were identified as potential key targets.
  • Database and single-cell analyses indicated MP exposure upregulates CDK1 in pulmonary fibroblasts, promoting fibrosis.

Conclusions:

  • Microplastic exposure acts as a cross-disease driving risk factor for COPD, IPF, and LUAD.
  • CDK1 is identified as a critical mediator in the pathogenesis of MP-related lung diseases.
  • This study provides a novel perspective on MP-induced lung pathogenesis and identifies CDK1 as a potential therapeutic target.