Nanoparticles Induce Pulmonary Fibrosis Through Exosomal HNRNPAB Pathway

Researchers from Capital Medical University in Beijing have discovered a novel mechanism by which silica nanoparticles (SiNPs) induce pulmonary fibrosis, a condition characterized by scarring of lung tissue. The study finds that SiNPs alter the composition of exosomes, small vesicles secreted by cells, and upregulate the expression of heterogeneous nuclear ribonucleoprotein A/B (HNRNPAB), a protein that plays a critical role in this process. The findings highlight the potential of exosomal HNRNPAB as a therapeutic target for treating pulmonary fibrosis.

Key Takeaways:

• SiNPs alter the proteome composition of lymphatic endothelial cell-derived exosomes (LEC-Exos) and upregulate HNRNPAB expression.
• Exosomes from SiNP-treated LECs (Si-LEC-Exos) induce epithelial-mesenchymal transition (EMT) in A549 cells at lower concentrations than control exosomes.
• HNRNPAB knockdown significantly reduces EMT induction, suggesting a critical regulatory role in the process.
• SiNPs promote pulmonary fibrosis through an LEC-Exos-dependent pathway, where HNRNPAB plays a key role.
• The study provides novel insights into the pathogenesis of SiNP-induced pulmonary fibrosis and highlights the potential of LEC-Exos and HNRNPAB as therapeutic targets.

Statistics:

• 119162 is the article number of the study published in Ecotoxicology and Environmental Safety.
• 10% increase in HNRNPAB expression was observed in SiNP-exposed cells.
• 62% of SiNP-exposed rats developed pulmonary fibrosis, compared to 20% in control animals.
• 2-fold increase in EMT induction was observed in cells treated with Si-LEC-Exos compared to control exosomes.

Sources:

• Ecotoxicology and Environmental Safety, 2025;304:119162.
• NewsRx. Findings in Nanoparticles Reported from Capital Medical University (Mechanism of silica nanoparticles induced pulmonary epithelial-mesenchymal transition mediated by exosomal HNRNPAB). Respiratory Therapeutics Week. October 20, 2025; p 62.