ArticleCardiovascular research2026
Gene expression profiles of carotid plaques differ between patients with amaurosis fugax and those with cerebral transient ischaemic attack or stroke.
Article in Cardiovascular research, 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
15 authors.
Funding
Abstract
aimsIn patients with atherosclerotic internal carotid artery stenosis, the risk of subsequent ischaemic stroke is higher in those presenting with a cerebral transient ischaemic attack (TIA) than in those with amaurosis fugax (AFX; transient monocular blindness). While AFX is associated with more stable histological characteristics, the underlying molecular mechanisms remain unclear. We hypothesized that biological processes and gene expression profiles in carotid plaques of patients with AFX differ from those with cerebral TIA and stroke. METHODS AND
resultsWe analysed carotid plaques from 2508 patients undergoing endarterectomy between 2002 and 2022. Bulk RNA sequencing (RNA-seq) was performed on 1088 plaques (136 asymptomatic, 179 AFX, 481 TIA, 292 stroke). Single-cell RNA-seq from 46 previously profiled plaques was used to identify cell-specific transcriptomic signatures. Mass spectrometry-based proteomics (n = 189) and targeted plasma proteomics (n = 1291) were used to validate the molecular differences. AFX plaques showed fewer lipid-rich cores than those from cerebral TIA [odds ratio (95% CI): 1.41 (1.03-1.94)] or stroke [1.42 (1.01-1.99)]. RNA-seq identified 408 differentially expressed genes (DEGs) between AFX and TIA and 463 between AFX and stroke (FDR < 0.1), while AFX and asymptomatic plaques showed only 10 DEGs. AFX plaques were enriched for vascular smooth muscle cell signatures and extracellular matrix remodelling, while cerebral TIA and stroke plaques exhibited macrophage-driven inflammatory molecular signatures. These transcriptomic differences were confirmed by plaque proteomic analyses. In parallel, circulating proteomic profiling revealed higher levels of inflammatory and thrombo-inflammatory markers in cerebral TIA and stroke compared with AFX.
conclusionAFX plaques exhibit stable, SMC-dominant molecular signatures that differ markedly from the macrophage-driven inflammatory profiles of cerebral TIA and stroke plaques. These findings support AFX as a biologically distinct entity with potential implications for risk stratification and personalized treatment.
Indexed as
Identifiers
What 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.