Obesity, inflammation, and atherosclerosis

By V. Z. Rocha, Peter Libby. Nature Reviews Cardiology, 2009

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Obesity and C‐reactive protein in various populations: a systematic review and meta‐analysis (2013, background): “In obesity, the accumulation of free fatty acid intermediates activates proinflammatory serine kinase cascades, such as IkB kinase and c-JunN-terminal kinase (16).”
INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, neutral): “…to contribute to pathology by amplifying recruitment of macrophages and other immune cells to atherosclerotic lesions and to influence processes that promote modifications of LDL that increase its uptake by macrophages and smooth muscle cells, such as oxidation (reviewed in Rocha and Libby, 2009).”
Obesity and inflammation: the linking mechanism and the complications (2016, background): “Moreover, accumulation of free fatty acids in obesity activates pro-inflammatory serine kinase cascades, such as I kB kinase and c-Jun N-terminal kinase, which in turn promotes adipose tissue to release IL-6 that triggers hepatocytes to synthesize and secrete CRP [25].”