The article examines new approaches to reducing the risk of dyslipidemia through the gut-heart axis, with an emphasis on trimethylamine N-oxide (TMAO). High levels of TMAO increase the expression of CD36 and scavenger receptor A on macrophages, which promotes uptake of oxidized LDL particles and foam cell formation, a key step in atherogenesis[1]. At the same time, TMAO reduces the expression of the ABCA1 transporter, which inhibits reverse cholesterol transport and worsens the development of atherosclerosis[1]. DMB reduces TMAO levels in mice fed a Western diet rich in choline and carnitine, thereby reducing foam cell formation and atherosclerotic lesions without changing cholesterol levels[1]. In aortic banding-induced heart failure models, DMB attenuates hypertrophy, fibrosis, inflammatory markers, and electrical remodeling[1]. The IMC inhibitor increases the excretion of neutral sterols in the stool, reduces the expression of the NPC1L1 transporter in the intestines, and prevents the accumulation of cholesterol in the liver[1]. IMC also improves renal function and reduces tubulointerstitial fibrosis in a murine model of chronic kidney disease induced by a choline diet[1].