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showed that TMAO not only promoted cellular inflammation but also accounted for oxidative stress, thus playing an indirect role in promoting expression of inflammatory cytokines ( In human umbilical vein endothelial cells (HUVECs) and aortas from ApoE -/- mice, TMAO increased the concentrations of reactive oxygen species (ROS), especially superoxide, by inhibiting the SIRT3-SOD2-mitochondrial ROS signaling pathway ( Endothelial dysfunction and thrombosis TMAO may lead to endothelial dysfunction

Violin, J

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These are proposed based on in vitro and rodent studies their relevance to human physiology is plausible but not validated through clinical research