不同的理论的Lp (a)会导致动脉粥样硬化。早期病变(1)Lp (a)进入血管壁和由MPO氧化,12/15,法律事务外包,NADPH, O₂ ⁻,和H₂O₂。(2)OxLp (a)和OxPLs构成实质性的单层通透性增加,导致增加Lp (a)和低密度脂蛋白进入血管壁。(3)OxLp (a)和OxPLs绑定到e前列腺素受体(EP2)受体,导致连接段沉积1 (CS-1)。此外,OxLp (a)刺激细胞粘附分子的表达(ICAM, VCAM E-selectin)绑定到单核细胞在内皮细胞表面。(4)OxLp (a)也可以激活特定disintegrin和金属蛋白酶(亚当斯)导致积极的肝素结合表皮生长因子的释放(HBEGF)和激活表皮生长因子受体(EGFR)和血管内皮生长因子受体2 (VEGFR2),导致引发和单核细胞趋化蛋白1 (MCP)生产。(5)这些吸引单核细胞的趋化因子简化访问到动脉壁。(6)OxPL积聚导致单核细胞分化成M1,树突细胞,这种细胞,和泡沫细胞。先进的病变(7)巨噬细胞吞噬OxLp (a)通过清道夫受体CD36形成泡沫细胞。(8)Ox-Lp (a)和Lp (a)也引起异常增殖,迁移,表型转换的平滑肌细胞(smc)。(9)OxLp (a)刺激CD36 TLR2/6激活,激活ERK和导致ER应激线粒体的完整性丧失,最终导致细胞凋亡。 (10) Apoptotic cells provide more OxPLs and stimulate angiogenesis. (11) OxLp(a) may stimulate LKB1/AMPK/ mTOR activity and induce apoptotic cell removal by macrophages. (12) Necrotic core formation and vessel wall rupture. (13) Macrophage and OxLp(a) cause increased platelet aggregation. (14) Apo(a) binding to PLG binding sites blocks the interaction between PLG and tissue PLG activator (tPA). (15) Lp(a) increases the production and activity of tPA inhibitor-1 (PAI-1), which eventually leads to a decrease in fibrinolysis (16). Lp(a) increases the expression of TF and inhibits the potent inhibitory effect of tissue factor pathway inhibitor (TFPI), which leads to thrombosis. Dotted lines: hypothesized pathways.