Zingg Jean-Marc, Vlad Adelina, Ricciarelli Roberta
Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Physiology Department, "Carol Davila" UMPh, 020021 Bucharest, Romania.
Antioxidants (Basel). 2021 Jul 26;10(8):1184. doi: 10.3390/antiox10081184.
Levels of oxidized low-density lipoproteins (oxLDLs) are usually low in vivo but can increase whenever the balance between formation and scavenging of free radicals is impaired. Under normal conditions, uptake and degradation represent the physiological cellular response to oxLDL exposure. The uptake of oxLDLs is mediated by cell surface scavenger receptors that may also act as signaling molecules. Under conditions of atherosclerosis, monocytes/macrophages and vascular smooth muscle cells highly exposed to oxLDLs tend to convert to foam cells due to the intracellular accumulation of lipids. Moreover, the atherogenic process is accelerated by the increased expression of the scavenger receptors CD36, SR-BI, LOX-1, and SRA in response to high levels of oxLDL and oxidized lipids. In some respects, the effects of oxLDLs, involving cell proliferation, inflammation, apoptosis, adhesion, migration, senescence, and gene expression, can be seen as an adaptive response to the rise of free radicals in the vascular system. Unlike highly reactive radicals, circulating oxLDLs may signal to cells at more distant sites and possibly trigger a systemic antioxidant defense, thus elevating the role of oxLDLs to that of signaling molecules with physiological relevance.
氧化型低密度脂蛋白（oxLDL）在体内的水平通常较低，但只要自由基生成与清除之间的平衡受到破坏，其水平就会升高。在正常情况下，摄取和降解是细胞对oxLDL暴露的生理反应。oxLDL的摄取由细胞表面清道夫受体介导，这些受体也可能作为信号分子发挥作用。在动脉粥样硬化的情况下，高度暴露于oxLDL的单核细胞/巨噬细胞和血管平滑肌细胞由于细胞内脂质积累而倾向于转化为泡沫细胞。此外，清道夫受体CD36、SR-BI、LOX-1和SRA的表达增加会加速动脉粥样硬化进程，以应对高水平的oxLDL和氧化脂质。在某些方面，oxLDL的作用，包括细胞增殖、炎症、凋亡、黏附、迁移、衰老和基因表达，可被视为对血管系统中自由基增加的适应性反应。与高反应性自由基不同，循环中的oxLDL可能向更远距离的细胞发出信号，并可能触发全身抗氧化防御，从而将oxLDL的作用提升到具有生理相关性的信号分子的作用。
