Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance.

By J. Odegaard, R. Ricardo-Gonzalez, Alex Red Eagle, Divya Vats, Christine R. Morel, Matthew H. Goforth, V. Subramanian, Lata Mukundan, A. Ferrante, A. Chawla. Cell Metabolism, 2008

876 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/53c2dd095c181e28fd7666c68ae93c03eea7d459

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Citations in the corpus

Regulation of learning and memory by meningeal immunity: a key role for IL-4 (2010, background): “This striking Th2 skewing of the T cell phenotype pointed to a potential alternative (M2) mode of activation of meningeal myeloid cells by these T cells (Kang et al., 2008; Martinez et al., 2008; Odegaard et al., 2008).”
INTERLEUKIN-4- AND INTERLEUKIN-13-MEDIATED ALTERNATIVELY ACTIVATED MACROPHAGES: ROLES IN HOMEOSTASIS AND DISEASE (2013, positive): “Subsequently, the maintenance of AAMs in WAT was found to be dependent on macrophage-intrinsic PPARγ and IL-4/IL-13–STAT6 signals, likely derived from WAT-associated eosinophils; reduction of either cell type in vivo resulted in diet-induced metabolic dysregulation characterized by insulin resistanc”
Macrophage death and defective inflammation resolution in atherosclerosis (2009, background): “In this context, a deficiency in PPARδ and/or its activators in advanced lesions could increase the M1/M2 ratio and decrease efferocytosi”
Macrophage plasticity and polarization: in vivo veritas. (2012, positive): “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).”
The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “For example, in response to IL-4, PPAR-δ directs Kupffer cells to express an alternative macrophage phenotype, thereby ameliorating obesity-induced insulin resistanc”
Mitochondria in the regulation of innate and adaptive immunity (2015, positive): “Furthermore, the loss of the transcription factors of the peroxisome proliferator-activated receptor (PPAR) family, transcription factors known to activate oxidative metabolism in numerous tissues, leads to a deficit in M2 polarization (Kang et al., 2008; Odegaard et al., 2007, 2008).”
Understanding the Mysterious M2 Macrophage through Activation Markers and Effector Mechanisms (2015, background): “The M2 macrophages are sources of neurotransmitters and hormones, such as catecholamines [120], substance P [121], adiponectin [122], and growth factors [123].”
Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders (2016, background): “org April 2016 | Volume 7 | Article 30 Activation of M2 ATMs by Th2 cytokines, such as IL-4, attenuates the pro-inflammatory response in inflamed adipose tissues and ameliorates metabolic complications, including insulin resistance (146, 172).”