Abstract
Background and Aims: Triglyceride-rich lipoproteins (TRLs) are an independent risk factor for atherosclerotic cardiovascular disease (CVD). Monocyte-derived macrophages are regulators of the atherosclerotic process. We recently showed that monocytes can adopt a long-term pro-inflammatory phenotype upon brief stimulation with atherogenic stimuli, such as oxidized LDL. This is termed trained immunity. We hypothesized that a single high-fat challenge induces trained immunity, which could contribute to the atherogenic effects of transient postprandial TRL elevations.
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