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TMAO-induced inflammation and endothelial dysfunction in human umbilical vein endothelial cells (HUVECs) can be reversed by treatment with the ROS inhibitor N-acetylcysteine (NAC) or by siRNA-mediated knockdown of NLRP3, suggesting that TMAO exerts its pro-inflammatory effects via the ROS/NLRP3 inflammasome [146]
Heinecke, JW Cholesterol accumulation regulates expression of macrophage proteins implicated in proteolysis and complement activation Arterioscler Thromb Vasc Biol 32 12: 2910-8
Nucleus 3, 433441
