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- W2945278503 abstract "Abstract Atherosclerosis is characterized by a persistent, low-grade inflammation of the arterial wall. Monocytes and monocyte-derived macrophages play a pivotal role in the various stages of atherosclerosis. In the past few years, metabolic reprogramming has been identified as an important controller of myeloid cell activation status. In addition, metabolic and epigenetic reprogramming are key regulatory mechanisms of trained immunity, which denotes the non-specific innate immune memory that can develop after brief stimulation of monocytes with microbial or non-microbial stimuli. In this review, we build the case that metabolic reprogramming of monocytes and macrophages, and trained immunity in particular, contribute to the pathophysiology of atherosclerosis. We discuss the specific metabolic adaptations, including changes in glycolysis, oxidative phosphorylation, and cholesterol metabolism, that have been reported in atherogenic milieus in vitro and in vivo. In addition, we will focus on the role of these metabolic pathways in the development of trained immunity." @default.
- W2945278503 created "2019-05-29" @default.
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- W2945278503 creator A5041039861 @default.
- W2945278503 creator A5050515977 @default.
- W2945278503 date "2019-05-03" @default.
- W2945278503 modified "2023-09-23" @default.
- W2945278503 title "Immunometabolism orchestrates training of innate immunity in atherosclerosis" @default.
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- W2945278503 doi "https://doi.org/10.1093/cvr/cvz107" @default.
- W2945278503 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6910162" @default.
- W2945278503 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31050710" @default.
- W2945278503 hasPublicationYear "2019" @default.
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