FIGURE 2.

Effects of gut microbiota and its metabolites on atherosclerosis, myocardial infarction, heart failure and hypertension. The interaction between diet and gut microbiota may promote the development of cardiovascular disease through common and different mechanisms. Western food rich in red meat promotes the production of TMA by bacteria, which is oxidized to TMAO in liver. TMAO may participate in atherosclerosis by interfering with cholesterol transport, foam cell formation and platelet aggregation. The effect of TMAO on blood pressure was mainly manifested in its enhancement of pressure-raizing effect of Ang II. Platelet aggregation also plays a role in atherosclerosis. The decrease of dietary fiber is related to the decrease of bacterial production of SCFAs, which play an immunomodulatory role in intestinal mucosa. The decrease of SCFAs level can promote local inflammation, aggravate intestinal ecological imbalance, and lead to the damage of intestinal barrier function. The damage of intestinal barrier function leads to the leakage of bacterial toxins, which further aggravates local and systemic inflammation. In addition, dysbiosis destroys the intestinal mucosal barrier, leading to gut microbiota entering the systemic circulation, which increases the incidence of adverse cardiovascular events after MI and aggravates the progress of HF. The roles of gut microbiota and its metabolites in hypertension.