ArticleFrontiers in toxicology2026
Polymer-specific nanoplastics trigger oxidative stress, inflammatory activation, and mitoepigenetic remodeling:
Article in Frontiers in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Recent studies have detected nanoplastics (NPs) in human tissues and biological fluids, raising concerns regarding their potential effects on cellular homeostasis. Nevertheless, their effects on mitochondrial regulation and mitoepigenetic processes remain poorly understood. This work aimed to study the polymer-specific effects of NPs, including polystyrene (PS), polypropylene (PP), and polyvinyl chloride (PVC), on mitochondrial function, mitochondrial homeostasis, oxidative stress generation, inflammatory response, and mitoepigenetics. Methods: Cell uptake of NPs was examined using flow cytometry and fluorescence microscopy. Analysis of mitochondrial membrane potential (Δψm), oxidative phosphorylation (OXPHOS), Mitochondrial reactive oxygen species (mtROS) generation, respiratory chain complexes, DNA damage repair enzymes, DNA methylation-related markers, inflammatory cytokines, and mitochondrial gene expression was performed at different time points after NP treatment. Moreover, docking analysis was performed to investigate the potential interactions between oxidized nanoplastic-derived oligomers and mitochondrial Complex I. The relationship between respiratory chain function and mtDNA expression was analyzed using regression. Results: The observed effects of the tested NPs included specific effects of each polymer type, such as increased mtROS production, reduced Δψm, induction of oxidative DNA damage, dysregulation of mitochondrial dynamics, and activation of inflammatory pathways. The stress response was characterized by downregulation of DNA methyltransferases, changes in methylation marker levels, and alterations in mitochondrial gene expression. Functional analysis identified Complex I as particularly vulnerable to the effects of NP treatment. The correlation study demonstrated the coordinated regulation of stress-response mediators in mitochondria, namely, DRP1, OMA1, DELE1, and MT-ND6. Meanwhile, the regression analysis showed a correlation between MT-ND6 expression and Complex I activity. Discussion: Collectively, these findings suggest that environmentally relevant NPs elicit polymer-dependent mitochondrial stress responses, mitoepigenetic remodeling, and inflammatory activation.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.