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• W2000251574 abstract "Significant attention has focused on the role of low-density lipoprotein (LDL) in the pathogenesis of atherosclerosis. However, recent advances have identified triglyceride-rich lipoproteins [e.g., very LDL (VLDL)] as independent risk predictors for this disease. We have previously demonstrated peroxisome proliferator-activated receptor (PPAR)δ, but not PPARγ, is the major nuclear VLDL sensor in the macrophage, which is a crucial component of the atherosclerotic lesion. Here, we show that, in addition to β-oxidation and energy dissipation, activation of PPARδ by VLDL particles induces key genes involved in carnitine biosynthesis and lipid mobilization mediated by a recently identified TG lipase, transport secretion protein 2 (also named desnutrin, iPLA2ζ, and adipose triglyceride lipase), resulting in increased fatty acid catabolism. Unexpectedly, deletion of PPARδ results in derepression of target gene expression, a phenotype similar to that of ligand activation, suggesting that unliganded PPARδ suppresses fatty acid utilization through active repression, which is reversed upon ligand binding. This unique transcriptional mechanism assures a tight control of the homeostasis of VLDL-derived fatty acid and provides a therapeutic target for other lipid-related disorders, including dyslipidemia and diabetes, in addition to coronary artery disease." @default.
• W2000251574 created "2016-06-24" @default.
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• W2000251574 date "2006-02-07" @default.
• W2000251574 modified "2023-09-23" @default.
• W2000251574 title "Peroxisome proliferator-activated receptor δ promotes very low-density lipoprotein-derived fatty acid catabolism in the macrophage" @default.
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• W2000251574 doi "https://doi.org/10.1073/pnas.0510815103" @default.
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