TABLE 6.

Main metabolites of gut microbiota related to CHD.

Metabolites of gut microbiota	Possible mechanism of action	References
TMAO	Upregulating scavenger receptor expression in macrophages Increasing the expression of cellular Heat shock protein (HSPs) Increasing the expression of proinflammatory cytokine Increasing plasma cholesterol levels Contributing to platelet hyperreactivity and enhancing the potential for thrombosis	(14, 19, 20)
Short-chain fatty acids (SCFAs)	Regulating renin secretion and blood pressure Regulating the expression of intercellular adhesion molecules and improving vascular endothelial function Lowering energy intake by promoting the production of anorectic hormones Stimulating the synthesis of bile acids Reducing the expression of pro-inflammatory factors to regulate the occurrence of inflammation	(21–26)
Secondary bile acids (SBAs)	Regulating systemic lipid and glucose metabolism Reducing the release of pro-inflammatory factors	(27, 28)
Lipopolysaccharide (LPS)	Inducing formation of foam cell and lipid accumulation to accelerate AS Exerting a pro-inflammatory effect leading to increased blood pressure Increasing platelet activation	(29–31)
Phenylacetylglutamine (PAGln)	Fostering platelet responsiveness and thrombosis potential via adrenergic receptors	(32)