很多人体检时，体检出颈动脉粥样斑块，询问为什么会得？
Pathophysiological mechanism of atherosclerosis. (1) LDL particles penetrate deep into the arterial wall, where they are oxidized by reactive oxygen species (ROS) to oxLDL. (2) At the site of arterial endothelial injury, monocyte recruitment occurs. (3) The VLA-4 receptor binds to the adhesion molecules, allowing monocytes to migrate into the arterial wall. (4) Depending on the microenvironment, monocytes transform into either proinflammatory or anti-inflammatory macrophages.(5) Proinflammatory macrophages engulf oxLDL particles, while the locally produced macrophage colony-stimulating factor (M-CSF) enhances their chemotactic and phagocytic activity. (6) Macrophages packed with oxLDL become foam cells. (7) Naive T-lymphocytes migrate into the atherosclerotic plaque, where their activation and clonal expansion mainly into Th1 lymphocytes ensues. (8) Vascular smooth muscle cells proliferate and migrate to the forming core of the atherosclerotic plaque. (9) Over time, atherosclerotic plaque builds up in the vessel wall. (10) Thrombus forms at the site of plaque rupture. (11) Ultimately, the cells disintegrate, forming a necrotic core.
动脉粥样硬化的病理生理机制。(1) LDL颗粒深入动脉壁，在动脉壁被活性氧(ROS)氧化为oxLDL。(2)在动脉内皮损伤部位，发生单核细胞募集。(3) vla4受体与粘附分子结合，使单核细胞迁移到动脉壁内。(4)根据微环境的不同，单核细胞可以转化为促炎或抗炎巨噬细胞。(5)促炎巨噬细胞吞噬oxLDL颗粒，而局部产生的巨噬细胞集落刺激因子(M-CSF)增强其趋化和吞噬活性。(6)被oxLDL包裹的巨噬细胞变成泡沫细胞。(7)幼稚t淋巴细胞迁移到动脉粥样硬化斑块，随后它们的活化和克隆扩增主要进入Th1淋巴细胞。(8)血管平滑肌细胞增殖并向动脉粥样硬化斑块形成核心迁移。(9)随着时间的推移，动脉粥样硬化斑块在血管壁上积聚。(10)在斑块破裂处形成血栓。最终，细胞瓦解，形成坏死的核心。
Antioxidants 2023, 12(5), 1083; https://doi.org/10.3390/antiox12051083
IF: 7.0 Q1 B2
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