ReviewArchives of toxicology2026
Microplastics induce mitochondrial dysfunction and accelerate cardiovascular pathogenesis.
Review in Archives of toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microplastics and nanoplastics (MNPs) are becoming ubiquitous environmental pollutants, with increasing evidence of their systemic toxicity. MNPs are increasingly detected in human tissues, including the cardiovascular system, and have been implicated in the pathogenesis of cardiovascular disease through mitochondrial dysfunction. This review integrates mechanistic insights into how MNPs impair mitochondrial integrity, induce oxidative stress, disrupt calcium signaling, and promote genomic instability in cardiac tissue. MNPs also exacerbate inflammation, cellular senescence, mitophagy dysfunction, and pro-atherosclerotic remodeling. Furthermore, this review examines sex-specific mitochondrial responses and developmental vulnerabilities. Understanding the molecular crosstalk between MNPs exposure and mitochondrial damage may provide a foundation for targeted interventions to mitigate environmental cardiovascular risks.
Indexed as
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What OpenQuestion 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 OpenQuestion graph.