LDL biochemical modifications: a link between atherosclerosis and aging.
LDL biochemical modifications: a link between atherosclerosis and aging.
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DOI：
10.3402/fnr.v59.29240
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发表时间：
2015
影响因子：
3.3
通讯作者：
Ramírez R
中科院分区：
文献类型：
--
作者：
Alique M;Luna C;Carracedo J;Ramírez R
动脉粥样硬化是一种以年龄增长为危险因素的老年性疾病。修饰的低密度脂蛋白(LDL)是众所周知的心血管疾病的危险标志物。体外和体内实验表明，高浓度的血浆低密度脂蛋白及其修饰，如氧化、糖基化、氨甲基化和糖氧化，都是致动脉粥样硬化的。动脉粥样硬化是由于活性氧(ROS)对动脉壁低密度脂蛋白的改变造成的。有证据表明，动脉粥样硬化的常见危险因素增加了内皮细胞和其他细胞产生游离ROS的可能性。此外，氧化应激是诱导内皮细胞衰老的重要因素。因此，内皮损伤和细胞衰老是动脉粥样硬化的公认标记物。本文综述了低密度脂蛋白的修饰，并讨论了衰老导致动脉粥样硬化的病理机制，包括内皮细胞损伤和氧化应激，以及衰老与动脉粥样硬化之间的联系。
Atherosclerosis is an aging disease in which increasing age is a risk factor. Modified low-density lipoprotein (LDL) is a well-known risk marker for cardiovascular disease. High-plasma LDL concentrations and modifications, such as oxidation, glycosylation, carbamylation and glycoxidation, have been shown to be proatherogenic experimentally in vitro and in vivo. Atherosclerosis results from alterations to LDL in the arterial wall by reactive oxygen species (ROS). Evidence suggests that common risk factors for atherosclerosis raise the likelihood that free ROS are produced from endothelial cells and other cells. Furthermore, oxidative stress is an important factor in the induction of endothelial senescence. Thus, endothelial damage and cellular senescence are well-established markers for atherosclerosis. This review examines LDL modifications and discusses the mechanisms of the pathology of atherosclerosis due to aging, including endothelial damage and oxidative stress, and the link between aging and atherosclerosis.