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Polyvinyl chloride nanoplastics induce lipid metabolism reprogramming of macrophages
Summary
This study found that polyvinyl chloride nanoplastics trigger lipid metabolism reprogramming in macrophages, promoting foam cell formation through a lipoprotein-mediated pathway, suggesting a potential mechanism linking nanoplastic exposure to cardiovascular disease risk.
Nanoplastics are increasingly detected in human tissues, yet their biological interactions and health effects remain poorly understood. Here, we show that polyvinyl chloride (PVC) nanoplastics change lipid metabolism of macrophages such as the induced formation of foam cells through a lipoprotein-mediated mechanism. Using transmission electron microscope, scattering light-confocal imaging, and soft X-ray nano-computed tomography, we visualize intracellular PVC nanoplastics and extensive lipid droplet accumulation in macrophages. Proteomic profiling reveals that PVC nanoplastics acquire apolipoproteins enriched protein corona, particularly ApoA1, imparting them with a lipoprotein-like identity. In response, macrophages selectively upregulate scavenger receptor class B type 1 (SR-B1), a key HDL receptor involved in cholesterol uptake and lipid homeostasis. These findings uncover a receptor-specific pathway by which apolipoprotein-coated nanoplastics mimic endogenous lipoproteins, disrupt lipid metabolism, and drive foam cell–like transformation. This work highlights uncovered links of the exposure of nanoplastics to cardiovascular risk through immune-metabolic reprogramming.