ArticleNature communications2025
MAT2A promotes atherosclerotic plaque vulnerability by mediating epigenetic reprogramming of macrophages.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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
1 citing paper in PubMed.
- Metabolic Perspective on Atherosclerosis: Macrophage Reprogramming and Novel Therapeutic Targets.Journal of the American Heart Association · 2026Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Atherosclerosis is mediated by circulating monocytes and lesional macrophages through chronic inflammation accompanied by metabolic reprogramming. Although methionine metabolism enhances the proinflammatory capacity of monocytes/macrophages, its role in atherosclerosis remains unclear. Here, we use untargeted metabolomics and mass spectrometry to demonstrate that monocyte methionine metabolism is associated with vulnerable plaque (thin-cap fibroatheroma [TCFA]) identified by pancoronary optical coherence tomography. Methionine adenosyltransferase Ⅱ alpha (MAT2A), the key enzyme of methionine metabolism, is highly expressed in atherosclerosis. Further epigenetic profiling of inflammatory and migratory gene promoters reveals MAT2A-mediated enrichment of the transcriptional permissive chromatin mark H3K4me3. Myeloid-specific MAT2A ablation and pharmacological inhibition, or a low-methionine diet, reduce monocyte/macrophage inflammation and migration, thereby attenuating plaque vulnerability. Mechanistically, norepinephrine activates the mTOR-c-MYC axis to upregulate MAT2A expression. The combination of norepinephrine and methionine metabolism is associated with TCFA presence and 5-year clinical prognosis. Consequently, MAT2A-mediated methionine metabolism represents a potential therapeutic target for atherosclerosis.
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Registered trials
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