Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways

Abstract Micro- and nanoplastics (MNPs), due to their widespread distribution and chemical stability, have emerged as novel environmental contaminants threatening cardiovascular health. Evidence links MNPs to conditions such as atherosclerosis, cardiac fibrosis, myocardial infarction, and other cardiovascular diseases (CVDs). Recently, MNPs have been found within atherosclerotic plaques and in the myocardial tissues of surgery patients, highlighting their close association with cardiovascular pathology. Investigations have demonstrated that MNPs can enter the human body through oral ingestion, inhalation, dermal contact, and medical procedures, and subsequently accumulate in the blood, blood vessels, and cardiac tissues. Once deposited, these particles induce oxidative and endoplasmic reticulum stress, disrupt mitochondrial function, and activate inflammatory signaling pathways, ultimately triggering cell death. These processes contribute to endothelial dysfunction, cardiac damage and fibrosis, vascular smooth muscle cell phenotypic switching, and macrophage foam cell formation, thereby likely contributing to the onset and progression of CVDs. Despite these findings, the potential cardiovascular risks of MNPs and the underlying mechanisms remain largely unexplored. This review summarizes the basic properties of MNPs, their biodistribution within the cardiovascular system, toxic effects, and underlying molecular mechanisms, providing a foundation for future risk assessment and the development of preventive strategies.