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Gut Microbiota and Its Metabolites in Atherosclerosis Development
Magdalena D Pieczynska1,2, Yang Yang1,3, S Petrykowski1
1Department of Molecular Biology, Institute of Genetics and Animal Breeding of the Polish Academy of Sciences, Postepu 36A Street, 05-552 Jastrzebiec, Poland.
Gut microbiota metabolites influence host health and nutrient absorption. Improving gut microbial diversity can help prevent and treat atherosclerosis by impacting lipid metabolism and inflammation.
Area of Science:
- Microbiology
- Nutrition Science
- Cardiovascular Research
Background:
- Gut microbiota metabolites significantly impact host digestive function and overall health.
- Intestinal microbes regulate host metabolism and nutrient absorption via serotonin, cytokines, and metabolites.
- Gut microbiota converts dietary polyphenols into absorbable bioactive substances, enhancing their activity.
Purpose of the Study:
- To summarize the effects of gut metabolites from natural products on atherosclerosis.
- To elucidate the mechanisms by which gut metabolites influence atherosclerosis development.
- To highlight the role of gut microbial metabolites in vascular health.
Main Methods:
- Literature review of studies on gut microbiota, metabolites, and atherosclerosis.
- Analysis of regulatory mechanisms involving serotonin, cytokines, and metabolites.
- Examination of the impact of polyphenols, prebiotics, and probiotics on gut microbiota.
Main Results:
- Gut microbial metabolites indirectly affect atherosclerosis by regulating lipid metabolism and inflammation.
- Reduced gut microbial diversity correlates negatively with atherosclerosis development.
- Gut metabolites directly impact vascular endothelial cells and macrophage foam cell formation.
Conclusions:
- Improving gut microbial diversity and number is a potential strategy for atherosclerosis prevention and treatment.
- Gut microbial metabolites play a crucial role in cardiovascular health.
- Natural products and dietary interventions can modulate gut microbiota for therapeutic benefits.
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