ArticleJournal of cardiovascular translational research2025
Identification of Plasma Lipidomic Signatures Associated with Coronary Plaque Vulnerability.
Article in Journal of cardiovascular translational research, 2025. 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
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
2 citing papers in PubMed.
- Sphingolipids in human disease: organ-specific pathologies, chain-length-dependent effects, and translational implications.Journal of translational medicine · 2026Review
- AI-driven identification of nutrition-modulated biomarkers and drug targets for cardiovascular therapeutic mechanisms.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
The objective of this study was to identify plasma lipid signatures associated with plaque vulnerability. We retrospectively evaluated coronary plaque in 99 patients using optical coherence tomography (OCT) and quantified 489 plasma lipids. We identified intra- and inter-class crosstalk among ceramide (Cer)-phosphatidylinositol (PI)-esterified cholesterol (CE)-sphingomyelin (SM) (Cer-PI-CE-SM) in patients with thin-cap fibroatheroma (TCFA). CE-16:0, SM d18:1/16:1, and GM3 d18:1/22:0, emerged as potential markers of TCFA, correlating with the thinnest fibrous cap thickness and the presence of cholesterol crystallization. Compared to the clinical model (area under the curve [AUC] = 0.810), the AUC of the combined clinical-lipid model improved [AUC = 0.880, p = 0.032]. Calibration and decision curves demonstrated that the combined model exhibited superior diagnostic performance. We identified lipid molecules that are strongly correlated with plaque vulnerability, thus providing an option for the non-invasive identification of vulnerable plaques, which could potentially facilitate the tailored treatment for high-risk patients.
Indexed as
Identifiers
40540208What Socratic 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 Socratic graph.