Transcriptomic biomarker analysis of micro- and nanoplastic induced cardiovascular toxicity reveals perturbations in mitochondrial and ribosomal networks

Environmental pollutants are increasingly recognized as major threats to human health worldwide with micro and nanoplastics (MNPs) outstanding on top, yet their contribution to cardiovascular disease (CVD) at the molecular level remains underexplored. In our study, we conducted an integrative bioinformatics analysis of human transcriptomic datasets to investigate the transcriptional alterations induced by MNP exposure. Differentially expressed genes revealed pervasive perturbations in pathways central to cardiovascular pathology, including oxidative stress, lipid metabolism, immune activation and mitochondrial functions. Protein-protein interaction networks and hub gene analysis identified mitochondrial genes such as MT-ND1 and COX5A , which were upregulated and linked to a potential mitochondrial stress signature requiring functional validation due to enhanced oxidative phosphorylation. On the other hand, ribosomal genes such as RPL5 were downregulated, suggesting impaired translational capacity and protein synthesis. This dual molecular mark, mitochondrial transcriptional regulation alongside ribosomal suppression highlights a coordinated cellular stress mechanism that could contribute to inflammation, remodeling, and energy imbalance in cardiovascular tissues. By mapping these signatures against cardiovascular associated gene sets, we demonstrated the MNP exposure converges molecular pathways already implicated in atherogenesis, cardiac remodeling, and vascular dysfunction. Importantly, transcription factor enrichment suggested upstream regulation by stress responsive factors, providing new insights into how plastic exposure may alter cellular homeostasis. Collectively, this work presents an integrative analysis linking transcriptomic signatures of human MNP exposed lung and intestinal cell models to curated cardiovascular disease gene sets. Our findings propose candidate hub genes and regulatory pathways for experimental validation and underscores the urgency of considering environmental plastic pollution into cardiovascular risk assessment, prevention, and therapeutic development.