APOE and atherosclerosis: Wu et al. found that treatment of TMAO damaged the structure and function of mitochondria in Apoe–/– mice via elevating the expression of succinate dehydrogenase complex B subunit, increasing the production of reactive oxygen species, promoting endothelial cell apoptosis, and enhancing the release of proinflammatory cytokines, thereby exacerbating atherosclerosis [30].