PPAR-γ dependent and independent effects on macrophage-gene expression in lipid metabolism and inflammation
By A. Chawla, Y. Barak, L. Nagy, D. Liao, P. Tontonoz, R. Evans. Nature Medicine, 2001
1,022 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/ce4c38001dffe2354e84096bbc06ad8f44b1dfa0
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Citations in the corpus
- The mechanisms of action of PPARs. (2002, result): “In general accordance with this conclusion, the Evans group recently utilized murine PPARγ null macrophages to demonstrate that previously reported inhibitory actions of PPARγ agonists on macrophage cytokine production occur via a receptor-independent mechanism (94).”
- Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation. (2006, methodology): “Embryonic stem cell-derived macrophages (ESDM) were cultured as described previously (Chawla et al., 2001), except with the following modifications.”
- Role of Microglia in Neurotrauma (2010, neutral): “PPARs are ligand-activated transcription factors of the nuclear hormone receptor family(182); activation of the PPAR isoform has demonstrated significant anti-inflammatory effects, including attenuation of proinflammatory cytokine, iNOS, and COX2 expression.(183) PPAR agonists, such as rosiglitazone”
- Emerging roles of PPARS in inflammation and immunity (2002, methodology): “This comes from the recent experiments by Chawla et al.(62), in which homologous recombination was used to create embryonic stem cells that have a null mutation of the gene encoding PPARγ.”