Sorting out the roles of PPARα in energy metabolism and vascular homeostasis

By P. Lefebvre, G. Chinetti, J. Fruchart, Bart Staels. 2006

831 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/1942e989e28932128cd5795673d97ae01dbd1ea7

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Citations in the corpus

Molecular mechanism of PPARα action and its impact on lipid metabolism, inflammation and fibrosis in non-alcoholic fatty liver disease. (2015, background): “acid oxidation (FAO) rates such as liver, heart, skeletal muscle, brown adipose tissue, and kidney, although it is also expressed in many tissues and cells including the intestine, vascular endothelium, smooth muscle and immune cells such as monocytes, macrophages and lymphocytes [3].”
Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, positive): “…is primarily involved in regulation of genes involved in fatty acid oxidation, ketogenesis, gluconeogenesis, cholesterol catabolism and lipoprotein metabolism (Lefebvre et al. 2006; Mandard et al. 2004), as well as anti-inflammatory genes (Michalik and Wahli 2008; Zandbergen and Plutzky 2007).”
International Union of Pharmacology. LXI. Peroxisome Proliferator-Activated Receptors (2006, background): “Consistent with its distribution in tissues with high catabolic rates of fatty acids and high peroxisomal activity, the major role of PPAR is the regulation of energy homeostasis (Lefebvre et al., 2006).”
Regulation of mTORC1 and its impact on gene expression at a glance (2013, background): “…activity of PPARa, a nuclear receptor that controls the expression of genes required for fatty acid oxidation and ketone body synthesis (reviewed by Lefebvre et al., 2006). mTORC1 impairs PPARa activity by promoting the nuclear accumulation of nuclear receptor corepressor 1 (nCoR1), a negative…”
The role of FoxO in the regulation of metabolism (2008, result): “PPARd, whose expression in skeletal muscle is greater than that of other family members, stimulates lipid metabolism and fatty acid oxidation, similar to the effects of FoxO1 described above (Lefebvre et al., 2006).”
The peroxisome proliferator-activated receptor: A family of nuclear receptors role in various diseases (2011, background): “[10,11] PPAR-α ligands can be both synthetic or endogenous FAs and FAderived compounds are natural ligands for PPAR-α.”