ArticleThrombosis journal2026
Urinary 11-dehydrothromboxane B2 as a dynamic biomarker of atherosclerotic thrombotic risk and its association with plaque instability.
Article in Thrombosis journal, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtherosclerosis is the main pathological basis of cardiovascular events. Urinary 11-dehydrothromboxane B 2 (11-dhTXB2), as a stable metabolite of Thromboxane (TX) A2, may reflect platelet activity and plaque stability, but its mechanism is not clear.
methodsA total of 160 patients with atherosclerosis were enrolled in this study. The correlation between urinary 11-dhTXB2 level and plaque morphology and inflammation index was detected. The effects of 11-dhTXB2 on macrophage polarization and endothelial barrier function were investigated by THP-1 macrophage and HUVEC co-culture model and ApoE
resultsHigh levels of urinary 11-dhTXB2 were significantly associated with thinner fibrous cap and increased inflammatory markers, especially in diabetic patients with atherosclerosis and aspirin resistance. Cell experiments showed that activation of the TXA2 pathway (as indicated by elevated urinary 11-dhTXB2) promoted macrophage M1 polarization and impaired endothelial connexin expression. The combination of curcumin and aspirin can synergistically reduce urinary 11-dhTXB2, reduce plaque area and improve plaque stability. Notably, urinary 11-dhTXB2 serves as a stable metabolite reflecting in vivo TXA2 production and platelet activation, but is not itself a functional ligand acting on macrophages or endothelial cells.
conclusionUrinary 11-dhTXB2 can be used as a dynamic monitoring biomarker for the risk of atherosclerotic thrombosis. Elevated TXA2 pathway activity aggravates plaque instability by promoting inflammation and endothelial dysfunction. Curcumin combined with aspirin has the potential for synergistic intervention and provides a new strategy for individualized prevention and treatment. CLINICAL TRIAL NUMBER: Not applicable.
Indexed as
Identifiers
42449382What 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.