ArticleBioactive materials2026
Artificial platelets suppressing deep vein thrombosis via competitive adhesion.
Article in Bioactive materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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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.
- Artificial intelligence for precision gene therapy: emerging technologies, clinical applications, and future directions.Frontiers in genetics · 2026Review
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deep vein thrombosis (DVT) remains a therapeutic challenge, primarily driven by pathological platelet adhesion at sites of vascular injury mediated by endothelial adhesion molecule overexpression. However, the molecular mechanisms underlying endothelial-dependent pathological platelet adhesion remain elusive. Here, integrating single-cell RNA sequencing (scRNA-seq) and functional validation, we identified aberrant activation of the stimulator of interferon genes (STING) as a critical driver of endothelial dysfunction and pathological platelet adhesion. Using STING knockout mice, we confirmed its central role in promoting a prothrombotic microenvironment via the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. Targeting this pathway, we identified forsythoside A (FA) as a potent STING inhibitor and constructed artificial platelets (Pm@Fng) via photopolymerization-membrane extrusion technology. Pm@Fng, consisting of FA-loaded nanogels cloaked with activated platelet membrane vesicles (APMVs), exhibited enhanced glycoprotein Ib alpha (GPIbα) -mediated binding affinity to von Willebrand factor (vWF), competitively blocking pathological platelet adhesion. Under thrombotic microenvironment (acidic pH and high reactive oxygen species), FA was released to modulate the STING - NLRP3 pathway, suppressing adhesion molecule expression. In a mouse DVT model, Pm@Fng rapidly targeted the endothelium, noticeably reducing thrombosis by 30% (p < 0.001) and preserving endothelial integrity. By exploiting competitive adhesion principles, this study presents a novel therapeutic strategy for DVT and other endothelial injury-related diseases.
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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 Socratic graph.