Dicks Leon M T
Department of Microbiology, Stellenbosch University, Private Bag X1, Matieland, Stellenbosch 7602, South Africa.
Int J Mol Sci. 2025 Aug 22;26(17):8142. doi: 10.3390/ijms26178142.
The internal mammary arteries (IMAs) and coronary arteries share many common characteristics. The inner layer (tunica intima, or intima) of both arteries is lined with a smooth, longitudinally orientated monolayer of endothelial cells (ECs), connective tissue, and an internal elastic lamina that separates the tunica intima from the tunica media (middle layer). The intima of IMAs is lined with an additional protective layer, the neointima, containing vascular smooth muscle cells (VSMCs). The neointima, located between the intima and internal elastic lamina, protects IMAs from damage by assisting in the remodeling of VSMCs. Coarse longitudinal folds in the internal elastic lamina of IMAs partially prevent the infiltration of VSMCs into damaged IMAs, and intimal thickening is thus less likely to occur. Inflamed IMAs resist the migration of monocytes across the endothelial layer and prevent the formation of lipid-rich macrophages (foam cells) within the subintimal or medial layers of arteries. IMAs are thus less likely to form plaques and develop atherosclerosis (AS). Higher levels of prostacyclin (PGI2) in IMAs prevent blood clotting. The anti-thrombotic agents, and production of tumor necrosis factor α (TNF-α), interferon-γ (INF-γ), and visfatin render IMAs more resistant to inflammation. An increase in the production of nitric oxide (NO) by ECs of IMAs may be due to small ubiquitin-like modifier (SUMO) proteins that alter the nuclear factor kappa B (NF-κB) and TLR pathways. The production of reactive oxygen species (ROS) in IMAs is suppressed due to the inhibition of NADPH oxidase (NOX) by a pigment epithelium-derived factor (PEDF), which is a serine protease inhibitor (SERPIN). In this review, a comparison is drawn between the anatomy of IMAs and coronary arteries, with an emphasis on how ECs of IMAs react to immunological changes, rendering them more suited for coronary artery bypass grafts (CABGs). This narrative review covers the most recent findings published in PubMed and Crossref databases.
乳内动脉（IMAs）和冠状动脉具有许多共同特征。这两种动脉的内层（内膜层，或内膜）都衬有一层光滑的、纵向排列的单层内皮细胞（ECs）、结缔组织以及将内膜层与中膜层（中间层）分隔开的内弹性膜。乳内动脉的内膜衬有一层额外的保护层——新生内膜，其中含有血管平滑肌细胞（VSMCs）。位于内膜和内弹性膜之间的新生内膜通过协助血管平滑肌细胞重塑来保护乳内动脉免受损伤。乳内动脉内弹性膜上的粗大纵向褶皱部分地阻止了血管平滑肌细胞浸润到受损的乳内动脉中，因此内膜增厚不太可能发生。发炎的乳内动脉可抵抗单核细胞穿过内皮细胞层的迁移，并防止在动脉内膜下或中膜层内形成富含脂质的巨噬细胞（泡沫细胞）。因此，乳内动脉形成斑块和发生动脉粥样硬化（AS）的可能性较小。乳内动脉中较高水平的前列环素（PGI2）可防止血液凝固。抗血栓形成剂以及肿瘤坏死因子α（TNF-α）、干扰素-γ（INF-γ）和内脂素的产生使乳内动脉对炎症更具抵抗力。乳内动脉内皮细胞产生的一氧化氮（NO）增加可能归因于小泛素样修饰物（SUMO）蛋白，这些蛋白会改变核因子κB（NF-κB）和Toll样受体（TLR）途径。由于色素上皮衍生因子（PEDF，一种丝氨酸蛋白酶抑制剂（SERPIN））对烟酰胺腺嘌呤二核苷酸磷酸氧化酶（NOX）的抑制作用，乳内动脉中活性氧（ROS）的产生受到抑制。在本综述中，对乳内动脉和冠状动脉的解剖结构进行了比较，重点关注乳内动脉内皮细胞如何对免疫变化做出反应，使其更适合冠状动脉旁路移植术（CABGs）。这篇叙述性综述涵盖了在PubMed和Crossref数据库中发表的最新研究结果。
