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Nano- and Microplastics in the Cardiovascular System: Current Insights and Biological Implications

Nanomaterials 2026
Mario Cristina, Manuel Belli, Anna Baroni, Chantalle Moulton, Emily Carinci, Marta Gatti, Ennio Tasciotti, Matteo Antonio Russo, P. Russo, Luigi Sansone

Summary

Tiny plastic particles from our environment—so small they can enter through the food we eat, the air we breathe, or even our skin—have been found lodged in heart and blood vessel tissue, and this review pulls together what scientists currently know about the damage they might cause, like inflammation, cell damage, and blood vessel problems that could contribute to heart disease. While researchers haven't yet proven these plastics directly cause heart disease in people, the growing evidence is concerning enough that the authors call for better tools to measure plastic exposure and more research into how to prevent harm. The bottom line: microplastics aren't just an environmental issue

Micro- and nanoplastics (MNPs) are ubiquitous environmental pollutants recognized as emerging and relevant risk factors for numerous human diseases, including cardiovascular diseases. MNPs enter the human body through ingestion, inhalation, and dermal penetration, and their toxicity varies according to size, shape, and chemical composition, most notably between microplastics (>1 µm) and nanoplastics (<1 µm), which differ in cellular uptake mechanisms and biodistribution. Recent evidence has confirmed their presence in cardiac and vascular tissues, raising significant concerns about their potential impact on human health. This review summarizes current knowledge on MNP exposure sources, physicochemical properties, and systemic bioavailability, with a particular emphasis on the mechanisms of transport that facilitate their deposition within the myocardium and vasculature. It further addresses a broad spectrum of cardiotoxic effects, including oxidative stress, mitochondrial injury, immune activation, ion channel disruption, cell death, and fibrosis. Endothelial dysfunction, vascular injury, and pro-atherogenic activity are also discussed. In addition to outlining existing detection techniques and emerging in vitro models, the review highlights initial steps toward the development of preventive strategies. Concluding with key knowledge gaps and future research directions, this article underscores the urgent need for standardized measurement tools, deeper insights into damage mechanisms, and clinical interventions to prevent MNP-induced cardiovascular diseases.

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