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. 2023 Feb 7;14:1085041. doi: 10.3389/fendo.2023.1085041

Figure 3.

Figure 3

The role of TMAO in onset and progression of atherosclerosis. High circulating levels of TMAO inhibited RCT, and accumulated cholesterol, which promoted the formation of foam cells; TMAO induced inflammatory responses, resulting in increased production of pro-inflammatory cytokines such as TNF-α and IL-1B; TMAO caused endothelial dysfunction and platelet activation, and ultimately contributed to the development of atherosclerosis.