ArticleiScience2026
Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- MicroRNA-425-5p as a diagnostic biomarker and ox-LDL-induced VSMC regulator in atherosclerosis.Journal of cardiothoracic surgery · 2026Article
- Extracellular vesicles inEXO : beyond the cell · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Visceral adipose tissue (VAT)-derived extracellular vesicles (EVs) have emerged as key mediators of inter-organ communication, yet their role in nicotine-induced atherosclerosis remains poorly defined. Here, we demonstrate that nicotine markedly enhances secretion of VAT-EVs and that these EVs are preferentially internalized by macrophages within atherosclerotic plaques, thereby accelerating lesion progression. Functionally, nicotine-induced VAT-EVs promote macrophage inflammation, oxidative stress, and foam cell formation. High-throughput profiling identified miR-210-3p as a dominant pro-atherogenic cargo within VAT-EVs, and its inhibition significantly attenuated nicotine-induced atherosclerosis
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Registered trials
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