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), sphingomyelin (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.

动脉粥样硬化性心血管疾病是全球主要的死亡原因之一。越来越多的证据表明，肠道微生物群 (GM) 及其代谢物在动脉粥样硬化 (AS)（现称为 GM 动脉轴）的发生和进展中起着关键作用。膳食脂质与转基因之间存在相互作用，最终影响转基因及其代谢物。鉴于这两个方面，GM-动脉轴可能在膳食脂质和 AS 之间发挥中介作用。富含饱和脂肪酸 (SFA)、omega-6 多不饱和脂肪酸 (n-6 PUFA)、工业反式脂肪酸 (TFA) 和胆固醇的饮食会增加致动脉粥样硬化微生物和代谢物的水平，而单不饱和脂肪酸 (MUFA) 、反刍动物 TFA 和植物甾醇 (PS) 可以增加抗动脉粥样硬化微生物和代谢物的水平。实际上，已证明膳食磷脂酰胆碱 (PC)、鞘磷脂 (SM) 和 omega-3 多不饱和脂肪酸 (n-3 PUFA) 通过 GM 动脉轴影响 AS。因此，GM-动脉轴充当膳食脂质和 AS 之间的沟通桥梁。在此，我们将描述 AS 中 GM 动脉轴的分子机制，并讨论膳食脂质与 GM 之间的复杂相互作用。特别是，我们将强调膳食脂质通过 GM 动脉轴影响 AS 的证据和潜在机制。我们将描述 AS 中 GM 动脉轴的分子机制，并讨论膳食脂质与 GM 之间的复杂相互作用。特别是，我们将强调膳食脂质通过 GM 动脉轴影响 AS 的证据和潜在机制。我们将描述 AS 中 GM 动脉轴的分子机制，并讨论膳食脂质与 GM 之间的复杂相互作用。特别是，我们将强调膳食脂质通过 GM 动脉轴影响 AS 的证据和潜在机制。