Gut microbiota and atherosclerosis

Atherosclerosis reflects a chronic inflammatory process of arteries. The origin of chronic vascular inflammation has been associated over a long time primarily with lipid disorders, but evidence from the past years has suggested that lipid-independent pathways are also involved. Recent research has demonstrated that the gastrointestinal microbiota has an impact on the development of atherosclerosis. Many clinical studies have revealed that there exist altered gut microbiota and increased intestinal abundance of bacteria from the oral cavity in atherosclerosis-related disorders such as cardiovascular disease or stroke, while several studies have demonstrated insights into underlying mechanisms. Various microbial-derived metabolites, such as the pathogen-associated molecular pattern endotoxin, trimethylamine N-oxide or imidazole propionate, contribute to atherosclerosis, while other bacterial metabolites, such as some tryptophan derivatives, might be protective. Furthermore, gut microbiota and lipid pathways are highly interactive, and the gut microbiota affects lipid absorption and storage, and the gut microbiota also contributes to vascular ageing. Interference with the gut microbiota by prebiotics, probiotics and antibiotics has demonstrated beneficial effects on atherosclerosis mainly in preclinical models. Overall, the gut microbiota has appeared as an important rheostat for vascular inflammation in atherosclerosis, which is controlled by host-microbe interactions that may be therapeutically exploited in the future.