ArticleFrontiers in immunology2026
Palmitic and oleic acids induce macrophage foam cell formation through C/EBPβ activation.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Abstract
Background: Foam cell formation is a critical early event in atherosclerosis. While oxidized low-density lipoprotein (oxLDL)-driven mechanisms are well studied, the contribution of free fatty acids (FFAs), particularly under high-fat dietary intake, is less defined. CCAAT/enhancer-binding protein β (C/EBPβ), a transcription factor regulating macrophage lipid metabolism, has been implicated, but its epigenetic role in FFA-induced lipid accumulation remains unclear. Methods: We exposed RAW 264.7 macrophages and mouse bone marrow-derived macrophages to palmitic and oleic acids to model FFA-driven foam cell formation Results: Exposure to palmitic and oleic acids markedly increased intracellular lipid content and induced upregulation of C/EBPβ and CD36. Chromatin profiling revealed C/EBPβ-dependent accessibility at promoters of genes involved in f atty acids uptake and storage. Silencing of C/EBPβ significantly reduced CD36 expression and lipid accumulation, attenuating foam cell formation. Conclusion: These findings establish a novel C/EBPβ-CD36 regulatory axis that drives FFA-induced foam cell formation through epigenetic remodeling. This mechanism provides new insight into dietary fatty acids-mediated macrophage reprogramming and suggests potential therapeutic targets for early atherosclerosis and lipid-driven cardiovascular disease.
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