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Updated: Jun 2, 2026
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.
Abstract:
Microplastics (MPs), as environmental pollutants, have garnered widespread attention. Growing evidence suggests a close association between MP exposure and lung diseases. However, the molecular mechanisms through which MP exposure influences the onset and progression of lung diseases remain unclear. This study positions MP exposure as a cross-disease driving risk factor and employs integrated computational toxicology and bioinformatics approaches to explore potential key targets underlying the impact of MP exposure on the development of lung diseases (COPD, IPF, and LUAD). Common differentially expressed genes (cDEGs) and shared common DEGs (scDEGs) associated with MP exposure and COPD, IPF, and LUAD were identified through database screening and intersection analysis. A protein-protein interaction (PPI) network was constructed using the STRING database, followed by enrichment analysis. The expression patterns and cellular localization of key targets among the shared common differentially expressed genes were validated using single-cell datasets of COPD, IPF, and LUAD. Finally, experimental validation was conducted based on the cell types identified through analysis. MP exposure may influence the occurrence and progression of COPD, IPF, and LUAD through mechanisms involving the cell cycle, mitosis, and DNA repair. Potential key targets identified include CDK1, BRCA1, and CCND1. Validation via database and single-cell analyses suggests that MP exposure may increase the risk of COPD, IPF, and LUAD by upregulating CDK1 expression in pulmonary fibroblasts. Experimental validation in human pulmonary fibroblasts demonstrated that PS-NPs significantly upregulated CDK1 mRNA and protein levels in a dose-dependent manner. CDK1 inhibition experiments confirmed that PS-NP exposure promotes fibrosis in human pulmonary fibroblasts by upregulating CDK1. This study defines MP exposure as a cross-disease driving risk factor and identifies CDK1 as a potential key target mediating the development of MPs-driven lung diseases. This finding offers a new perspective for understanding MPs-related lung diseases and establishes a novel paradigm for exploring the intrinsic connections between pollutant exposure and disease pathogenesis.
Insights
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:
- 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.
