ArticleACS nano2026
Microplastic-Induced Macrophage Dysfunction Drives Lung Tumor Progression through Glutathione Imbalance.
Article in ACS nano, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- Article
- Microplastics in Human Thoracic Tissues: Increased Burden in Patients with Lung Malignancy.Journal of clinical medicine · 2026Article
- Nanoplastics and Neurodegeneration: A Roadmap From Mechanism to Causation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Osteoimmunological impacts of micro/nanoplastics: systemic translocation, inflammatory responses, and bone remodeling disruption.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microplastics (MPs) are emerging contaminants whose immunological consequences remain poorly defined. Here, we investigated MP-induced immune responses using bone marrow-derived macrophages and a lung tumor model to delineate how MPs modulate tumor immunity. MPs triggered TLR2- and TLR4-dependent signaling pathways in macrophages, which initiated AP-1 signaling and lysosomal destabilization, followed by mitochondrial depolarization and excessive reactive oxygen species production. Despite NRF2 pathway activation, GPX1 and GPX3 were selectively suppressed, revealing a paradoxical uncoupling of glutathione metabolism that precipitated macrophage ferroptosis.
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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 OpenQuestion graph.