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A heart-on-a-chip simultaneously monitoring mechanical and electrophysiologic signals reveals charge-dependent micro/nano plastic cardiotoxicity
Summary
Scientists using a lab-made "heart-on-a-chip" found that tiny plastic particles (microplastics) can weaken heart cell function, and the particles' electrical charge matters a lot—positively charged plastic bits caused the most damage by disrupting calcium channels that help heart cells beat properly. This matters because microplastics are already being found in human blood and heart tissue, and this research suggests that not all plastic pollution poses equal risk—the charge on these particles, which can change as plastic breaks down in the environment, may be a key factor in how harmful they are to our hearts.
Environmental micro/nano plastics (MNPs) have recently been identified within the human circulation and myocardial tissues, yet the specific biophysical drivers of their toxicity remain poorly defined. While previous models have demonstrated general cardiotoxic effects, they typically utilize single-type particles that fail to account for the diverse surface charges acquired during environmental aging. Here, using a multimodal heart-on-a-chip platform, we show that the cardiotoxicity of polystyrene MNPs is strongly associated with their surface charge, with positive charged particles (pPS-MNPs) producing the most pronounced suppression of electromechanical function. Further, we observed that pPS-MNPs preferentially accumulate within cardiomyocytes and may physically interfere with L-type calcium channels (Cav1.2). This spatial association is consistent with the observed suppression of Ca transients and mitochondrial stress, and suggests a contribution of Cav1.2-associated Ca dysregulation to electromechanical impairment. Our findings, validated in a long-term rat exposure model, identify surface charge as a key determinant of MNP cardiotoxicity and highlight the necessity of charge-specific risk assessments for plastic pollution.