Institute of Histology and Embryology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Institute of Pathophysiology, Medical Faculty, University of Ljubljana, Ljubljana, Slovenia.
Bosn J Basic Med Sci. 2020 Feb 5;20(1):21-30. doi: 10.17305/bjbms.2019.4320.
Atherosclerosis is a chronic inflammatory disease of arteries and it affects the structure and function of all three layers of the coronary artery wall. Current theories suggest that the dysfunction of endothelial cells is one of the initial steps in the development of atherosclerosis. The view that the tunica intima normally consists of a single layer of endothelial cells attached to the subendothelial layer and internal elastic membrane has been questioned in recent years. The structure of intima changes with age and it becomes multilayered due to migration of smooth muscle cells from the media to intima. At this stage, the migration and proliferation of smooth muscle cells do not cause pathological changes in the intima. The multilayering of intima is classically considered to be an important stage in the development of atherosclerosis, but in fact atherosclerotic plaques develop only focally due to the interplay of various processes that involve the resident and invading inflammatory cells. The tunica media consists of multiple layers of smooth muscle cells that produce the extracellular matrix, and this layer normally does not contain microvessels. During the development of atherosclerosis, the microvessels from the tunica adventitia or from the lumen may penetrate thickened media to provide nutrition and oxygenation. According to some theories, the endothelial dysfunction of these nutritive vessels may significantly contribute to the atherosclerosis of coronary arteries. The adventitia contains fibroblasts, progenitor cells, immune cells, microvessels, and adrenergic nerves. The degree of inflammatory cell infiltration into the adventitia, which can lead to the formation of tertiary lymphoid organs, correlates with the severity of atherosclerotic plaques. Coronary arteries are surrounded by perivascular adipose tissue that also participates in the atherosclerotic process.
动脉粥样硬化是一种慢性动脉炎症性疾病，它影响冠状动脉壁的所有三层的结构和功能。目前的理论认为，内皮细胞功能障碍是动脉粥样硬化发展的初始步骤之一。近年来，人们对内膜通常由附着在血管内皮下层和内弹性膜上的单层内皮细胞组成的观点提出了质疑。内膜的结构随年龄而变化，由于平滑肌细胞从中膜迁移到内膜，内膜会变成多层。在这个阶段，平滑肌细胞的迁移和增殖不会引起内膜的病理变化。内膜的多层化被经典地认为是动脉粥样硬化发展的一个重要阶段，但实际上，由于涉及驻留和入侵炎症细胞的各种过程的相互作用，只有斑块才会在局部形成。中膜由产生细胞外基质的多层平滑肌细胞组成，该层通常不含微血管。在动脉粥样硬化的发展过程中，来自中膜外膜的微血管或来自管腔的微血管可能穿透增厚的中膜，为其提供营养和氧气。根据一些理论，这些营养血管的内皮功能障碍可能会显著促进冠状动脉的动脉粥样硬化。外膜包含成纤维细胞、祖细胞、免疫细胞、微血管和肾上腺素能神经。炎症细胞浸润外膜的程度，可能导致三级淋巴样器官的形成，与动脉粥样硬化斑块的严重程度相关。冠状动脉被血管周围脂肪组织环绕，后者也参与动脉粥样硬化过程。
