Abstract
Abstract Within atherosclerotic plaques, macrophages can take up cholesterol and thereby become lipid-laden cells. For long it has been thought that these foamy macrophages are the main contributors to chronic inflammatory responses in plaques. However, several publications lately highlighted that foamy plaque macrophages are less inflammatory than their non-foamy counterparts. Interestingly, a very recent EMBO Molecular Medicine paper by Wu et al. demonstrate that accumulation of lipids in tumor-associated macrophages (TAMs) elicits an immunosuppressive phenotype.
Highlights
Macrophage translates as “big eater”, from Greek and these innate immune cells engulf and kill microbes to protect us against infections
Foam cells are prevalent in all stages of atherosclerosis, leading to the common belief that they are the crucial drivers of chronic inflammation during this cholesterol-driven inflammatory disease
Wu and colleagues recently reported in EMBO Molecular Medicine that this immunosuppressive phenotype of Tumorassociated macrophages (TAMs) results from the accumulation of lipid droplets and associated metabolic rewiring [4]
Summary
Foam cells are prevalent in all stages of atherosclerosis, leading to the common belief that they are the crucial drivers of chronic inflammation during this cholesterol-driven inflammatory disease. Recent findings in cardiovascular research elicited a paradigm shift and highlight that “normal” macrophages, as opposed to lipid-laden foamy macrophages, are the main producers of inflammatory factors [1,2,3] (Figure 1). Lipid-laden macrophages gained attention outside the atherosclerosis field and crossed borders to cancer research.
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