Abstract
The intestinal microbiota is a marker of the organism state, capable of direct and indirect interacting. The main mechanisms underlying interactions are immunoregulation and energy metabolism. Metabolites, formed during the life of microbiota, realize their actions through these engagements. Some metabolites arouse negative effects on endothelial vessels, causing and maintaining a systemic inflammatory response, which stands behind major cardiac risk factors. Metabolites and molecules such as lipopolysaccharide or trimethylamine N-oxide initiate endothelial dysfunction, and thus trigger the processes of atherogenesis, insulin resistance and even increase blood pressure by activating inflammasomes and pro-inflammatory cytokines. Short-chain fatty acids including the main metabolites such as acetate, propionate and butyrate are antagonists of lipopolysaccharide and trimethylamine N-oxide. These substances are a source of energy for intestinal epithelial cells. They maintain homeostasis, stimulate the production of anti-inflammatory components and activating reparative processes. Another important factor influencing levels on blood pressure and systemic inflammation is intestinal barrier dysfunction, which is determined by the regulatory protein zonulin. Besides, there are proved receptor interactions, as well as qualitative and quantitative changes in the composition of the microbiota that can influence blood pressure and atherogenesis. Each cardiovascular disease is characterized by its own microbiological pattern and the predominance of specific metabolites. The article presents a review, summarizing experimental and clinical data on the role of microbiota in the development of atherosclerosis and cardiovascular diseases.