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Visceral white adipose tissue (WAT) regulates systemic lipid metabolism and inflammation. Dysfunctional WAT drives chronic inflammation and facilitates atherosclerosis. Adipose tissue macrophages (ATMs) are the predominant immune cells in WAT, but their heterogeneity and phenotypes are poorly defined during atherogenesis. The scavenger receptor CD36 mediates ATMs crosstalk with other cells, driving chronic inflammation. Here, we conducted single-cell RNA sequencing on major WAT ATM subpopulations using a diet-induced atherosclerotic mouse model ( Apoe -null). We also examined the role of CD36 using Apoe / Cd36 double-null mice. Our results indicate that ATMs are constantly under lipid stress. We identified lipid-associated macrophages (LAMs), which were previously described in obesity. Interestingly, LAMs increased 8.4-fold in Apoe / Cd36 double-null mice on an atherogenic diet, but not in Apoe -null mice. The increase in LAM was accompanied by more ATM lipid uptake, reduced adipocyte hypertrophy, and less inflammation, which indicate a delicate balance between lipid metabolism and inflammation, mediated through CD36.
Zhang et al. (Wed,) studied this question.
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