ReviewParticle and fibre toxicology2026
Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways.
Review in Particle and fibre 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
8 authors.
Funding
Abstract
Micro- and nanoplastics (MNPs), due to their widespread distribution and chemical stability, have emerged as novel environmental contaminants threatening cardiovascular health. Evidence links MNPs to conditions such as atherosclerosis, cardiac fibrosis, myocardial infarction, and other cardiovascular diseases (CVDs). Recently, MNPs have been found within atherosclerotic plaques and in the myocardial tissues of surgery patients, highlighting their close association with cardiovascular pathology. Investigations have demonstrated that MNPs can enter the human body through oral ingestion, inhalation, dermal contact, and medical procedures, and subsequently accumulate in the blood, blood vessels, and cardiac tissues. Once deposited, these particles induce oxidative and endoplasmic reticulum stress, disrupt mitochondrial function, and activate inflammatory signaling pathways, ultimately triggering cell death. These processes contribute to endothelial dysfunction, cardiac damage and fibrosis, vascular smooth muscle cell phenotypic switching, and macrophage foam cell formation, thereby likely contributing to the onset and progression of CVDs. Despite these findings, the potential cardiovascular risks of MNPs and the underlying mechanisms remain largely unexplored. This review summarizes the basic properties of MNPs, their biodistribution within the cardiovascular system, toxic effects, and underlying molecular mechanisms, providing a foundation for future risk assessment and the development of preventive strategies.
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.