Macrophage-specific PPARγ controls alternative activation and improves insulin resistance

By J. Odegaard, R. Ricardo-Gonzalez, Matthew H. Goforth, Christine R. Morel, V. Subramanian, Lata Mukundan, A. Eagle, Divya Vats, F. Brombacher, A. Ferrante and 1 more. Nature, 2007

2,157 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/9e2861a4d2733444e9c7e4382cf2b6423fb64c60

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Citations in the corpus

Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “In contrast, Th2 mediators (e.g., IL-4) drive the M2 phenotype, which activates expression of immunosuppressive factors and peroxisome proliferator-activated receptor gamma (PPARg) that promote tissue remodeling and helps resolve inflammation (Odegaard et al., 2007).”
Protective and pathogenic functions of macrophage subsets (2011, background): “These macrophages are induced by peroxisome proliferator activated receptor-γ (PPARγ) signalling and maintain adipocyte function, insulin sensitivity and glucose tolerance, which can prevent the development of diet-induced obesity and type 2 diabete”
Macrophage Polarization in Inflammatory Diseases (2014, background): “Many key transcription factors are involved in macrophage polarization [12] , like signal transducer and activator of transcription (STATs)[13], interferon-regulatory factor (IRFs) [14, 15] , nuclear factor (NF)-κB [16] , activator protein (AP) 1 [17] , peroxisome proliferator-activated receptor (PP”
Heterogeneity of Microglial Activation in the Innate Immune Response in the Brain (2009, background): “Increased mRNA expression is found for IL-10, TGF-β, CD23 (the low-affinity IgE receptor, FcεRII), insulin growth factor 1 (IGF-1), nerve growth factor (NGF), and peroxisome proliferation activation receptor gamma (PPAR-γ; Brodie et al. 1998; Table 2 Identifying features of microglial activation sta”
Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord (2009, background): “Peroxisome proliferatoractivated receptor agonists, used clinically to treat diabetes, also can promote M2 macrophage differentiation (Odegaard et al., 2007) and have been shown to be neuroprotective in preclinical models of SCI (McTigue et al., 2007).”
Krüppel-like factor 4 regulates macrophage polarization. (2011, methodology): “Sequence analysis revealed two consensus KLF-binding sites (CACCC) within a previously identified IL-4–responsive enhancer region of the Arg1 promoter (13, 30) (Figure 2E and Supplemental Figure 4C).”
The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “Macrophage-specific deletion of peroxisome proliferator–activated receptor-γ (PPAR-γ), a transcription factor that mediates anti-inflammatory and insulin-sensitizing effects, impairs AAM development, derepresses proinflammatory macrophage pathways and accentuates insulin resistance and glucose intol”
Macrophage plasticity and polarization: in vivo veritas. (2012, neutral): “Mice with macrophage-selective genetic inactivation of PPAR γ , PPAR δ , and KLF4 show inhibition of obesity-induced insulin resistance (19, 20, 24, 106, 110), although these results may be strain specific (112).”
Transcriptional regulation of macrophage polarization: enabling diversity with identity (2011, background): “More recent studies have shown that PPARγ-deficient macrophages are resistant to M2 polarization and promote insulin resistanc”