ArticleInflammation2026
Free Fatty Acids and LPS Synergistically Promote Macrophage M1 Polarization and Insulin Resistance Via FTO-Mediated CSF1 Degradation.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed.
- Natural Bioactive Compounds Targeting Gut Barrier Integrity and Metabolic Endotoxemia in Cardiometabolic Disease: Mechanistic Insights and Translational Perspectives.Molecules (Basel, Switzerland) · 2026Review
- The C-reactive protein-triglyceride-glucose index predicts new-onset atrial fibrillation after ST-segment elevation myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- FTO in cardiovascular diseases: mechanisms, context dependence, and translational opportunities.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Free fatty acids (FFA) and lipopolysaccharide (LPS) synergistically exacerbate metabolic inflammation, but the underlying mechanisms remain unclear. This study investigates how FFA and LPS cooperatively promote macrophage M1 polarization and insulin resistance (IR). In vivo models (HFD-fed and LPS-treated mice) and in vitro macrophage assays were employed. Flow cytometry, RNA-seq, m6A methylation analysis, and AAV-mediated gene modulation of FTO or CSF1 were used to dissect mechanisms. Metabolic phenotypes in mice were assessed via fasting blood glucose and HOMA-IR index. Combined FFA and LPS treatment synergistically increased M1 macrophage polarization and IR, correlating with elevated FTO expression. FTO upregulated by FFA/LPS reduced m6A modification of CSF1 mRNA, promoting its degradation via impaired IGF2BP2 binding. Depleting FTO or restoring CSF1 attenuated M1 polarization and improved insulin sensitivity in vivo. The FTO-m6A-CSF1 axis drives FFA/LPS-induced metabolic inflammation, offering therapeutic targets for IR.
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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.