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Conversely, TMAO can release inflammatory factors (caspase-1, IL-1 ) (49) in a dose-and time-dependent manner by activating the reactive oxygen species (ROS)thioredoxin-interacting protein (TXNIP) NLRP3 signaling pathway (50) and inhibiting sirtun3 (SIRT3) superoxide dismutase2 (SOD2)mitochondrial ROS signaling pathway (51), thereby causing endothelial cell injury and aggravating the formation and development of atherosclerosis

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