PPARs at the crossroads of lipid signaling and inflammation.
By W. Wahli, L. Michalik. Trends in endocrinology and metabolism, 2012
637 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/1a91b640d9607544ce26eeaa89ca0b08621a503b
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
- Lauren E Tebay
- Jennifer Lippincott-Schwartz
- A. Dinkova-Kostova
- Steve Vitale
- Sarah Cohen
- J. Hayes
- Trevor M. Penning
- Angelika S. Rambold
In Molecular Biology
- A. Dinkova-Kostova
- Angelika S. Rambold
- J. Hayes
- Lauren E Tebay
- Jennifer Lippincott-Schwartz
- Steve Vitale
- Sarah Cohen
- Pradeep K. Singh
Citations in the corpus
- Fatty acid trafficking in starved cells: regulation by lipid droplet lipolysis, autophagy and mitochondrial fusion dynamics (2015, background): “In addition, because FAs and their derivatives play important roles in regulating cellular signaling cascades and contribute to FAdriven modulations in metabolism, inflammatory responses, and cell death programs (Calder, 2013; Wahli and Michalik, 2012; Zechner et al., 2012), alterations in their lev”
- Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “…p62 and PPARg Limit Inflammation during ''Metabolic Activation'' The induction of PPARg in proinflammatory MMe macrophages seemed surprising given that saturated FFAs are poor PPARg ligands (Wahli and Michalik, 2012) and that PPARg exerts antiinflammatory effects (Odegaard et al., 2007).”
- Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease (2015, positive): “A contributing factor to the increased sensitivity of Nrf2−/− mice to inflammation may be loss of peroxisome proliferator-activated receptor γ (Pparγ) because it is known that Nrf2 positively regulates Pparγ [185] and that Pparγ exerts strong anti-inflammatory effects [186].”