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The gut microbiota-artery axis: A bridge between dietary lipids and atherosclerosis?

Journal

PROGRESS IN LIPID RESEARCH
Volume 89, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.plipres.2022.101209

Keywords

Dietary lipids; Atherosclerosis; Gut microbiota; Gut microbiota metabolites; Gut microbiota-artery axis

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Atherosclerotic cardiovascular disease is a major global cause of death, and the gut microbiota and its metabolites are now known to play a pivotal role in its onset and progression, forming the GM-artery axis. There are interactions between dietary lipids and the gut microbiota, which ultimately affect atherosclerosis. The GM-artery axis acts as a communication bridge between dietary lipids and atherosclerosis.
Atherosclerotic cardiovascular disease is one of the major leading global causes of death. Growing evidence has demonstrated that gut microbiota (GM) and its metabolites play a pivotal role in the onset and progression of atherosclerosis (AS), now known as GM-artery axis. There are interactions between dietary lipids and GM, which ultimately affect GM and its metabolites. Given these two aspects, the GM-artery axis may play a mediating role between dietary lipids and AS. Diets rich in saturated fatty acids (SFAs), omega-6 polyunsaturated fatty acids (n-6 PUFAs), industrial trans fatty acids (TFAs), and cholesterol can increase the levels of atherogenic microbes and metabolites, whereas monounsaturated fatty acids (MUFAs), ruminant TFAs, and phytosterols (PS) can increase the levels of antiatherogenic microbes and metabolites. Actually, dietary phosphatidylcholine (PC), sphingo-myelin (SM), and omega-3 polyunsaturated fatty acids (n-3 PUFAs) have been demonstrated to affect AS via the GM-artery axis. Therefore, that GM-artery axis acts as a communication bridge between dietary lipids and AS. Herein, we will describe the molecular mechanism of GM-artery axis in AS and discuss the complex interactions between dietary lipids and GM. In particular, we will highlight the evidence and potential mechanisms of dietary lipids affecting AS via GM-artery axis.

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