Illustration depicting microplastics accelerating atherosclerosis in male mice, contrasting with unaffected female mice, in a UC Riverside lab setting.
Illustration depicting microplastics accelerating atherosclerosis in male mice, contrasting with unaffected female mice, in a UC Riverside lab setting.
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Microplastics accelerate atherosclerosis in male mice, UC Riverside–led study finds

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A University of California, Riverside team reports that everyday microplastic exposure sped the buildup of arterial plaque in male—but not female—mice, pointing to possible sex-specific cardiovascular risks and endothelial cell vulnerability. The effects occurred without changes in body weight or cholesterol.

Researchers at the University of California, Riverside found that routine exposure to microplastics accelerated atherosclerosis in a well-established mouse model, with effects limited to males. The study adds to evidence that ubiquitous plastic particles may directly harm vascular health. (news.ucr.edu)

In work published November 17, 2025, in Environment International, investigators used LDL receptor–deficient mice maintained on a low-fat, low-cholesterol diet. Both sexes received oral microplastics at 10 milligrams per kilogram of body weight daily for nine weeks—an "environmentally relevant" level intended to approximate human exposures. (sciencedaily.com)

The exposure markedly worsened plaque only in males: a 63% increase in the aortic root and a 624% increase in the brachiocephalic artery. Females showed no significant progression. The team also reported no increases in body weight or blood lipids in either sex, suggesting the effect was independent of traditional risk factors. (sciencedaily.com)

Analyses pointed to endothelial cells—the inner lining of arteries—as a key target. Single-cell RNA sequencing showed altered cell composition and pro-atherogenic gene programs, and fluorescent particles were seen within plaques and concentrated in the endothelial layer. In vitro experiments indicated similar gene-activation responses in mouse and human endothelial cells. (sciencedaily.com)

The mouse findings align with emerging human data. Microplastics and nanoplastics have been detected in carotid atheromas, and in a 2024 New England Journal of Medicine study, patients whose plaques contained these materials had a 4.5-fold higher risk of heart attack, stroke, or death over about three years than those without them. Separate analyses have also found higher concentrations of microplastics in arteries bearing plaques than in plaque-free aortas. (reuters.com)

“Endothelial cells were the most affected,” said lead author Changcheng Zhou, a professor at UCR’s School of Medicine, who added that hormone-related factors, including estrogen, may help explain the sex difference observed in mice. The team plans to probe mechanisms, particle types and sizes, and whether similar patterns appear in people. (news.ucr.edu)

Zhou noted there is currently no way to remove microplastics from the body; he advised reducing exposure by limiting plastic food and water containers, cutting single-use plastics, and avoiding highly processed foods. (sciencedaily.com)

Collaborators included researchers at Boston Children’s Hospital/Harvard Medical School and the University of New Mexico Health Sciences. The work received partial support from the National Institutes of Health. The paper is titled “Microplastic exposure elicits sex-specific atherosclerosis development in lean low-density lipoprotein receptor-deficient mice.” (news.ucr.edu)

Hva folk sier

Initial reactions on X focus on the UC Riverside study's finding that microplastics accelerate atherosclerosis in male mice but not females, without changes in weight or cholesterol. Users express concern over potential human cardiovascular risks from everyday exposure. Official university posts promote the research, while some highlight endothelial cell dysfunction. Skeptical views challenge the lipid-heart hypothesis, suggesting microplastics as a key factor. Overall sentiment is neutral to alarmed, urging reduced exposure.

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