Trimethylamine N-oxide promotes oxidative stress and lipid accumulation in macrophage foam cells via the Nrf2/ABCA1 pathway.

Recently, trimethylamine N-oxide (TMAO) has been considered a risk factor for cardiovascular disease and has a proatherogenic effect. Many studies have found that TMAO is involved in plaque oxidative stress and lipid metabolism, but the specific mechanism is still unclear. In our study, meta-analysis and bioinformatic analysis were firstly conducted in the database, and found that the effect of high plasma TMAO levels on promoting atherosclerotic plaque may be related to the expression of key antioxidant genes nuclear factor erytheroid-derived-2-like 2 (NFE2L2/Nrf2) decreased.

Effect of autophagy on ferroptosis in foam cells via Nrf2.

The progression of atherosclerotic plaque is accelerated by death of foam cells during the development of the plaque. There are several forms of foam cell death, such as autophagy and ferroptosis forms of cell death together are commonly predominant. Therefore, it is particularly important to study the crosstalk between various forms of cell death in atheroscler and ferroptosis.