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Review Articles

LDL biochemical modifications: a link between atherosclerosis and aging

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Article: 29240 | Received 22 Jul 2015, Accepted 12 Nov 2015, Published online: 03 Dec 2015

Figures & data

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. 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 LDL double modification. The glycation of LDL particles renders it more prone to oxidation.

Fig. 2 LDL double modification. The glycation of LDL particles renders it more prone to oxidation.

Fig. 3 Mechanisms of endothelial cell senescence during aging, initiating the atherogenic process.

Fig. 3 Mechanisms of endothelial cell senescence during aging, initiating the atherogenic process.