Polyethylene and Polyvinyl Chloride Nanoplastics Accelerate Atherosclerosis Through Distinct Smooth Muscle Cell...

Area of Science:

• Environmental Health
• Cardiovascular Biology
• Toxicology

Background:

• Micro- and nanoplastics (MNPs) are prevalent in human tissues, but their cardiovascular impact is unclear.
• Polyethylene (PE) and polyvinyl chloride (PVC) are common in human atheromas, necessitating investigation into their atherogenic potential.

Purpose of the Study:

• To investigate the causal role of oral PE and PVC exposure in accelerating atherosclerosis.
• To elucidate the distinct molecular mechanisms by which PE and PVC affect vascular smooth muscle cells (SMCs) and contribute to cardiovascular disease.

Main Methods:

• Utilized ApoE-/- mice as a model for atherosclerosis.
• Administered PE and PVC orally to assess their impact on plaque development.
• Employed single-cell transcriptomic profiling to analyze SMC phenotypic changes.
• Examined transcriptional signatures in human carotid plaques for clinical relevance.

Main Results:

• Both PE and PVC exposure accelerated atherosclerosis, increasing plaque burden and reducing SMC markers.
• PE exposure induced SMCs to adopt a chondromyocyte-like cell (CMC) state, promoting osteogenic signaling and vascular calcification.
• PVC exposure promoted a fibromyocyte-like program, altering collagen metabolism and cell migration without calcification.
• Distinct SMC responses to PE and PVC were mirrored in human atherosclerotic plaques.

Conclusions:

• Establishes a causal link between common environmental plastics (PE, PVC) and accelerated atherosclerosis.
• Demonstrates that MNP-induced vascular risk is mediated by polymer-specific SMC fate decisions.
• Provides a mechanistic basis for understanding the cardiovascular risks of plastic pollution and potential therapeutic targets.