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Despite the complexity of TMAOs role in atherosclerosis, studies have indicated that managing TMAO through nutrition, medication, or microbiome modification may help lessen its effects and even reverse its contribution to the advancement of the disease [73, 76]
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For example, in pulmonary MVECs exposed to chronic IH, ROS production increased and was associated with endothelial barrier dysfunction due to ROS-dependent activation of extracellular signal-regulated kinases (ERK) 1/2 and c-Jun N-terminal kinases that initiate the reorganization of cytoskeletal and junctional proteins [154]
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