Peroxisome Proliferator-Activated Receptors

This study shows PPARγ suppresses cytosolic DNA-induced macrophage inflammation by reprogramming metabolism and inhibiting inflammatory gene expression through super-enhancer remodeling.

This study examines pemafibrate's tissue-specific transcriptional effects in PPAR-dependent mice, showing strong responses in liver and jejunum but not in other tissues.

This study develops a mathematical model of PPARγ dynamics to show stress-induced adipogenic commitment is a bistable, irreversible process regulated by circadian rhythms.

This study investigates the role of PPAR-γ in dexamethasone-induced osteogenic differentiation of human BMSCs, finding no significant effect of PPAR-γ inhibition on SOX9 or RUNX2 levels.

This study shows CDC14 phosphatases regulate adipogenesis by dephosphorylating PPARγ, improving glucose metabolism and preventing obesity in mice.

This paper identifies a small molecule inhibitor of PPARγ acetylation that improves insulin sensitivity and browning of white adipose tissue without the side effects of traditional PPARγ agonists.

PPARgene 2.0 updates the database with new PPAR target genes and improves prediction using language models and ChIP-seq data.

This study investigates the role of PPAR-delta versus PPAR-gamma in modulating central carbon metabolism during adipogenesis in human adipocytes using real-time qPCR and metabolic arrays.

This study identifies PPARα as a regulator of liver proteostasis, showing it suppresses protein synthesis and secretion while enhancing proteasome activity and degradation.

This study shows that trifluoroacetate reduces plasma lipids and atherosclerosis in mice by activating PPAR-alpha, but also highlights its environmental and clinical relevance.

This study shows EHMT1 and EHMT2 regulate adipogenesis and inflammation by controlling gene expression and histone modifications, with EHMT1 governing PPAR and EHMT2 affecting H3K9me2 levels.

The paper identifies key genes involved in NCSC adipogenesis through mRNA sequencing, RT-qPCR, and RNAi, revealing a positive feedback loop between C/EBPβ and PPARγ.

The paper identifies miR-223 as a key regulator of TBT-induced adipogenesis in MSCs and its transgenerational role in obesity.

The paper identifies PPAR activation as a key driver of compensatory renal proximal tubule hypertrophy using multi-omic analyses in a mouse model.

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 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.

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