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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Environmental Sources Human Health Effects Nanoplastics Sign in to save

PVC nanoplastics impair cardiac function via lysosomal and mitochondrial dysfunction

Biochemical and Biophysical Research Communications 2025 7 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 63 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Guoxia Liu, Qimei Bao, Chunkai Zhang, Yuke Zhong, Mingcong Deng, Yixing Huang, Zu Ye, Jing Ji, Jing Ji

Summary

Researchers found that PVC nanoplastics damaged heart cells by disrupting two critical cellular structures: lysosomes (the cell's recycling system) and mitochondria (the cell's energy producers). The nanoplastics caused lysosomes to become leaky and mitochondria to malfunction, leading to heart cell injury and impaired cardiac function. This study is concerning because PVC is one of the most common plastics, and the findings suggest that nanoplastic exposure could contribute to heart disease.

Polymers
Body Systems

MICRO: and nanoplastics (MNPs) are emerging environmental pollutants that pose a significant threat to human health, with traces found in cardiac tissues. While previous studies have indicated that MNPs can cantribute to cardiac dysfunction, there is limited systematic investigation into how MNPs exposure affects various organelles. This study focuses on polyvinyl chloride nanoparticles (PVC NPs), one of the most common and persistent plastic pollutants in the environment. Our findings reveal that PVC NPs engage in organelle-specific interactions, predominantly accumulating in the lysosomes and mitochondria of cardiomyocytes. This targeted accumulation results in substantial disruptions to lysosomal autophagic flux and mitochondrial energy metabolism. These results offer new insights into the organelle-specific mechanisms behind PVC NP-induced cardiotoxicity, highlighting the distinct risks associated with this widespread environmental contaminant.

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