JNK Expression by Macrophages Promotes Obesity-Induced Insulin Resistance and Inflammation

By M. Han, D. Jung, Caroline Morel, S. Lakhani, Jason K. Kim, R. Flavell, R. Davis. Science, 2013

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How researchers see this paper

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Obesity, Inflammation, Toll-Like Receptor 4 and Fatty Acids (2018, background): “These findings suggest that activation through JNK is an important mechanism linked to insulin resistance in obese patients [48].”
Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “Moreover, targeting pathways that mediate inflammation in the macrophage revealed significant roles for TLR4, JNK, and IKKb in potentiating ATM inflammation and insulin resistance in mice (Arkan et al., 2005; Han et al., 2013; Saberi et al., 2009).”
TNF and MAP kinase signaling pathways (2014, neutral): “Mechanistic studies of macrophages demonstrate that the requirement of JNK for Tnfα expression reflects a defect in macrophage polarization [88].”
Hepatic Acetyl CoA Links Adipose Tissue Inflammation to Hepatic Insulin Resistance and Type 2 Diabetes (2015, neutral): “, 2005; Suganami and Ogawa, 2010), and protection from inflammation-associated insulin resistance could explain the preserved insulin sensitivity of macrophage-specific c-JUN N-terminal kinase (m4JNK) knockout mice fed a high-fat diet (Han et al., 2013).”
Cellular and Molecular Players in Adipose Tissue Inflammation in the Development of Obesity-induced Insulin Resistance (2013, neutral): “total and CD11c ATM numbers and the pro-inflammatory gene expression in AT [126].”