ArticleFrontiers in molecular biosciences2026
Spatial localization of arachidonic acid in human carotid atherosclerotic plaques reveals a pro-inflammatory metabolic program in macrophages.
Article in Frontiers in molecular biosciences, 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
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Carotid atherosclerosis is a significant cause of ischemic stroke. It is a chronic inflammatory disease characterized by the progressive accumulation of inflammatory cells and mediators. Specific key metabolites are known to play pivotal roles in the progression of atherosclerosis. By applying spatial omics, we pinpointed the colocalization of arachidonic acid with inflammatory cells in plaques, providing direct spatial evidence for its pro-inflammatory role in atherosclerosis. Methods: We employed metabolomics, spatial metabolomics, and single-cell transcriptomics to compare human stable and unstable plaques, aiming to identify key molecules associated with atherosclerotic disease progression. The spatial distribution of key metabolites and lipid components was analyzed using matrix-assisted laser desorption/ionization mass spectrometry imaging, enabling a detailed description of their spatial characteristics within carotid atherosclerotic plaques. Results: Collected human carotid artery atherosclerotic plaque tissues via carotid endarterectomy (CEA) for metabolomic analysis, identifying 74 differential metabolites. Notably, the pro-inflammatory lipid arachidonic acid (AA) was involved in 22 of these pathways and was upregulated in unstable plaques. ROC curve analysis further indicated that AA had good predictive capability for the disease. Focused on investigating the metabolic processes of AA. Using spatial metabolomics technology, revealed the dynamic spatial distribution of the "linoleic acid-AA-leukotriene D4" metabolic axis within atherosclerotic plaques. Based on the pro-inflammatory properties of AA, further explored its spatial distribution within plaques and its association with macrophages. Through single-cell sequencing analysis of macrophage subsets, found that Conclusion: Our study provides direct spatial evidence for the existence of the "linoleic acid-AA-leukotriene D4" metabolic axis. It reveals the association of
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.