Dicks Leon M T
Department of Microbiology, Stellenbosch University, Private Bag X1, Matieland, Stellenbosch 7602, South Africa.
Int J Mol Sci. 2025 Sep 17;26(18):9052. doi: 10.3390/ijms26189052.
Atherosclerosis (AS), the leading cause of cardiovascular disease (CVD), is the thickening and stiffening of arterial walls, mainly of coronary arteries, the aorta, and the internal carotid artery. Blood flow is restricted by the deposit of lipid-rich macrophages (foam cells), calcium, fibrin, and cellular debris into plaques on the inner lining (tunica intima) of arterial walls. Damaged endothelia become inflamed and accumulate macrophages, monocytes, granulocytes, and dendritic cells, which intensifies plaque formation and increases the risk of myocardial infarction (MI) and thrombosis. Many of the anatomical and physiological abnormalities in arterial walls can be linked to colonic bacteria that produce inflammation-inducing metabolites, e.g., succinate, fumarate, fatty acids (FAs), reactive oxygen species (ROS), lipopolysaccharides (LPS), and trimethylamine-N-oxide (TMAO). TMAO triggers platelet formation, inhibits the synthesis of bile acids (BAs), accelerates the formation of aortic lesions, and upregulates the expression of membrane glycoprotein CD36 (also known as platelet glycoprotein 4) on the surface of platelets and epithelial cells. The ability of internal mammary arteries (IMAs) to produce higher levels of apolipoprotein C-III (apo-CIII) and paraoxonase (PON), compared to coronary arteries, prevents plaque buildup. The tunica intima of IMAs is rich in heparin sulfate and endothelial nitric oxide synthase (eNOS). Increased production of NO relaxes VSMCs and suppresses GTP cyclohydrolase (GTPCH), which lowers blood pressure. Higher levels of prostacyclin (PG12) produced by IMAs inhibit platelet aggregation. IMAs are structurally different from coronary arteries by having a thinner, non-fenestrated, tunica intima without a prominent internal elastic lamina. These characteristics render IMAs ideal conduits in coronary artery bypass graft (CABG) surgery. This review provides information that may explain why IMAs are less affected by inflammatory reactions and more resilient to plaque formation.
动脉粥样硬化（AS）是心血管疾病（CVD）的主要病因，表现为动脉壁增厚和变硬，主要累及冠状动脉、主动脉和颈内动脉。富含脂质的巨噬细胞（泡沫细胞）、钙、纤维蛋白和细胞碎片沉积在动脉壁内膜（内膜层）的斑块中，限制了血流。受损的内皮细胞发炎，积聚巨噬细胞、单核细胞、粒细胞和树突状细胞，这加剧了斑块形成，并增加了心肌梗死（MI）和血栓形成的风险。动脉壁中的许多解剖和生理异常可与产生炎症诱导代谢物的结肠细菌相关联，例如琥珀酸盐、富马酸盐、脂肪酸（FAs）、活性氧（ROS）、脂多糖（LPS）和三甲胺 - N - 氧化物（TMAO）。TMAO触发血小板形成，抑制胆汁酸（BAs）的合成，加速主动脉病变的形成，并上调血小板和上皮细胞表面膜糖蛋白CD36（也称为血小板糖蛋白4）的表达。与冠状动脉相比，乳内动脉（IMA）产生更高水平载脂蛋白C - III（apo - CIII）和对氧磷酶（PON）的能力可防止斑块形成。IMA的内膜富含硫酸乙酰肝素和内皮型一氧化氮合酶（eNOS）。一氧化氮产量增加可使血管平滑肌细胞（VSMC）舒张并抑制鸟苷三磷酸环水解酶（GTPCH），从而降低血压。IMA产生的较高水平前列环素（PGI2）可抑制血小板聚集。IMA在结构上与冠状动脉不同，其内膜较薄、无窗孔且无明显的内弹性膜。这些特性使IMA成为冠状动脉旁路移植术（CABG）中理想的血管。本综述提供的信息可能解释了为什么IMA受炎症反应影响较小且对斑块形成更具抵抗力。
