ArticleiScience2026
The Trojan Horse system composed of platelet membrane and extracellular vesicles inhibits atherosclerotic plaque progression.
Article in iScience, 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
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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
1 citing paper in PubMed.
- Post-Traumatic Stress Disorder and Atherosclerosis: Co-Phenomena, or Cause-and-Effect?Current atherosclerosis reports · 2026Review
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carotid atherosclerotic plaques are a leading cause of ischemic stroke and present a major challenge for early atherosclerosis intervention. Here we engineer a biomimetic delivery platform, such as the Trojan Horse system, composed of platelet membrane and extracellular vesicles (EVs) derived from M2-like macrophages. The resulting vesicles, called platelet-extracellular vesicles (P-EVs), selectively accumulate at injured endothelium and atherosclerotic plaques and enable the co-delivery of PIM1 siRNA and Max-40279. This strategy suppresses endothelial-mesenchymal transition, reduces macrophage foam cell formation, and attenuates inflammatory responses in lesions. In mouse models of atherosclerosis, treatment with P-EVs significantly limits plaque progression. These results establish P-EVs as a targeted approach for modulating vascular inflammation and provide a potential strategy for slowing atherosclerotic plaque development.
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Registered trials
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