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. 2015 Dec 3:59:29240.
doi: 10.3402/fnr.v59.29240. eCollection 2015.

LDL biochemical modifications: a link between atherosclerosis and aging

Matilde Alique  1 , Carlos Luna  2 , Julia Carracedo  2 , Rafael Ramírez  3
Affiliations

LDL biochemical modifications: a link between atherosclerosis and aging

Matilde Alique et al. Food Nutr Res. .

Abstract

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.

Keywords: LDL modifications; aging; atherosclerosis; endothelial damage; oxidative stress.

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Figures

Fig. 1
Fig. 1
LDL modifications. (a) Oxidation: oxidized product-induced native LDL oxidation and modifications of apoB amino acids. (b) Glycosylation: modification of LDL and apoB by advanced glycosylation end-products (AGEs). (c) Carbamylation: cyanate from urea, which binds to NH2 groups in proteins – inducing their carbamylation – is generated by spontaneous dissociation from urea.
Fig. 2
Fig. 2
LDL double modification. The glycation of LDL particles renders it more prone to oxidation.
Fig. 3
Fig. 3
Mechanisms of endothelial cell senescence during aging, initiating the atherogenic process.
See this image and copyright information in PMC

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