ArticleParticle and fibre toxicology2024
Acute exposure to polystyrene nanoparticles promotes liver injury by inducing mitochondrial ROS-dependent necroptosis and augmenting macrophage-hepatocyte crosstalk.
Article in Particle and fibre toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Nanoplastic Particle Exposure Induces Toxicity and Amplifies Cellular Stress in THP-1 Macrophages: Insights on Molecular Pathways and Circulating Proteome Interaction.Journal of biochemical and molecular toxicology · 2026Article
- Microplastics, nanoplastics and liver disease: an emerging health concern?Nature reviews. Gastroenterology & hepatology · 2026Review
- Micro- and Nanoplastics as Emerging Drivers of Liver Injury: Exposure, Evidence, and Mechanisms.International journal of molecular sciences · 2026Review
- Nrf2-dependent redox regulation protects myoblasts from polystyrene nanoplastic-induced premature senescence.Genes & genomics · 2026Article
- Review
- Article
- Polyethylene terephthalate microplastics impair erectile function through macrophage mediated cGAS-STING ferroptosis.iScience · 2026Article
- Polystyrene nanoplastics and benzo(a)pyrene synergistically induce lung fibrosis and inflammation via relaxin signalling in mice.Communications biology · 2026Article
- Glycine alleviates ovarian granulosa cell ferroptosis induced by ERα-mediated internalization of polystyrene microplastics.Communications biology · 2026Article
- Polyethylene glycol functionalization modulates the toxicity of zinc oxide quantum dots: a multilevel characterization and toxicological study of Channa punctatus Bloch.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Impact of nanoplastics emitted from incineration of polyethylene plastic on THP-1 macrophage viability and immune function.Journal of hazardous materials · 2026Article
- Environmental co-exposure to microplastics and phenol may influence redox signaling and tumor microenvironment dynamics.Journal of Cancer · 2026Review
- Pak4-mediated crosstalk between necroptotic macrophages and tendon stem/progenitor cells contributes to traumatic heterotopic ossification formation.Bone research · 2025Article
- Ferroptosis as a key player in the pathogenesis and intervention therapy in liver injury: focusing on drug-induced hepatotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte.Journal of nanobiotechnology · 2025Article
- Large-sized polystyrene microplastics induce oxidative stress in AML12 cells.Scientific reports · 2025Article
- Combined Effects of Nano-Polystyrene and Heavy Metal Mixture on the Bioaccumulation of Heavy Metals and Physiological Changes inJournal of xenobiotics · 2025Article
- Nanotechnology in Hematology: Enhancing Therapeutic Efficacy With Nanoparticles.Health science reports · 2025Article
- Oral Exposure to Nylon-11 and Polystyrene Nanoplastics During Early-Life in Rats.Nanomaterials (Basel, Switzerland) · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundThe global use of plastic materials has undergone rapid expansion, resulting in the substantial generation of degraded and synthetic microplastics and nanoplastics (MNPs), which have the potential to impose significant environmental burdens and cause harmful effects on living organisms. Despite this, the detrimental impacts of MNPs exposure towards host cells and tissues have not been thoroughly characterized.
resultsIn the present study, we have elucidated a previously unidentified hepatotoxic effect of 20 nm synthetic polystyrene nanoparticles (PSNPs), rather than larger PS beads, by selectively inducing necroptosis in macrophages. Mechanistically, 20 nm PSNPs were rapidly internalized by macrophages and accumulated in the mitochondria, where they disrupted mitochondrial integrity, leading to heightened production of mitochondrial reactive oxygen species (mtROS). This elevated mtROS generation essentially triggered necroptosis in macrophages, resulting in enhanced crosstalk with hepatocytes, ultimately leading to hepatocyte damage. Additionally, it was demonstrated that PSNPs induced necroptosis and promoted acute liver injury in mice. This harmful effect was significantly mitigated by the administration of a necroptosis inhibitor or systemic depletion of macrophages prior to PSNPs injection.
conclusionCollectively, our study suggests a profound toxicity of environmental PSNP exposure by triggering macrophage necroptosis, which in turn induces hepatotoxicity via intercellular crosstalk between macrophages and hepatocytes in the hepatic microenvironment.
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