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Editorial
. 2017 Oct 13;121(9):1024-1026.
doi: 10.1161/CIRCRESAHA.117.311923.

Liver Kinase B1 Links Macrophage Metabolism Sensing and Atherosclerosis

Vishal Kothari  1 , Karin E Bornfeldt  2
Affiliations
Editorial

Liver Kinase B1 Links Macrophage Metabolism Sensing and Atherosclerosis

Vishal Kothari et al. Circ Res. .
No abstract available

Keywords: Editorials; atherosclerosis; foam cells; glycolysis; lipid metabolism; macrophages; metabolism.

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Figures

Figure 1
Figure 1. Schematic representation of some of the effects of the metabolic sensor LKB1 in macrophages
In the atherosclerotic lesion, in areas where nutrients are sufficient, increased inflammatory mediators and modified LDL cause reduced LKB1 levels through LKB1 degradation in macrophages. Loss of LKB1 in turn reduces serine phosphorylation (p-S53) and subsequent lysosomal degradation of scavenger receptor A (SRA), which associate with increased uptake of modified lipoproteins, increased foam cell formation, and increased inflammatory activation of macrophages in response to inflammatory mediators. Inflammatory mediators also increase glycolysis and downstream metabolic processes required for the macrophage to mount a full immune response. In a nutrient deprived state, on the other hand, glycolysis and levels of glycolytic intermediated are low, and the LKB1 pathway is activated to preserve cellular energy. The cell is impaired in its ability to respond to inflammatory stimuli. LKB1 thus may act as a rheostat to allow the lesional macrophage to respond appropriately depending on its nutritional state.
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References

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