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914 Mechanistically, TMAO was able to accelerate the progression of atherosclerosis by inducing vascular endothelial cells (VECs) pyroptosis through SDHB/ROS pathway, 15 contribute to endothelial dysfunction by increasing HMGB1 expression and disrupting cell-cell junction proteins, 16 promote vascular calcification by inducing osteogenic differentiation of vascular smooth muscle cells (VSMCs) via NLRP3 inflammasome and NF-B pathway, 17 and exacerbate cardiac function and cardiac fibrosis after MI by promoting the transition of fibroblasts into myofibroblasts through TGF-RI/Smad2 axis

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