Peroxisome Proliferator-Activated Receptors

The paper identifies a dynamic HIF1alpha-PPARgamma circuit that both promotes and represses lipid accumulation during adipogenesis, revealing a mechanism for adipocyte dysfunction in obesity.

The paper uses BoNE to identify dual PPARα/γ agonism as a therapeutic strategy for IBD, validated in preclinical models and patient-derived cells.

This study compares the effects of GQ-16, a PPARγ partial agonist, and pioglitazone, a PPARγ full agonist, in treating nephrotic syndrome in rats, finding that GQ-16 reduces proteinuria and co-morbidities with fewer adipogenic side effects.

The paper shows that Pparα and fatty acid oxidation coordinate hepatic transcriptional architecture during fasting, with Ppar driving enhancer priming and acetylation independent of fatty acid oxidation.

This study identifies PPARγ as a regulator of Nprc gene expression in adipocytes through long-range enhancers, linking it to diet-induced changes in adipose tissue.

The paper models the PPAR pathway using a Bayesian approach to identify sub-pathways involved in HFD-induced obesity and suggests potential therapeutic targets.

The paper identifies PLAAT3 loss-of-function mutations in humans causing lipodystrophy and insulin resistance by impairing arachidonic acid-mediated PPAR signaling in adipose tissue.

This study investigates how PPARβδ ligands modulate inflammation in rat lung tissues, finding that agonists promote pro-inflammatory effects while antagonist-agonist combinations induce anti-inflammatory responses.

This study shows MED1 is essential for postnatal adipose expansion and de novo lipogenesis gene induction in mice, but not for adipose development or early adipogenesis.

This study identifies an upstream open reading frame (uORF) in the 5' UTR of chicken PPARγ1 that represses its translation.

The paper investigates how different PGC-1α isoforms regulate hepatic metabolism and apoptosis in response to inflammation, identifying distinct roles for PGC-11 and PGC-14.

This study investigates how PPARβ/δ inverse agonists repress transcription by recruiting NCOR and interfering with transcription factor recruitment.