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. 2018 Dec 6;23:101066. doi: 10.1016/j.redox.2018.101066

Fig. 5.

Fig. 5

Physiological effects of lipoxidized lipoproteins, with consequences for the immune system, inflammation, apoptosis and HDL function. (1) Oxidized LDL stimulates the production of antibodies against itself and oxidized phospholipids, that can be recognized by the immune system; (2) oxLDL and MDA-LDL bind to scavenger receptors, leading to their internalization and formation of foam cells; oxPC-Lp(a) promotes the expression of IL-8 by macrophages, increasing inflammation; (3) HNE-LDL leads to apoptosis by both inhibition the ubiquitin proteasome pathway and by modification of tyrosine kinase receptors, leading to their inhibition; (4) Acrolein-HDL inhibits the increase of HDL caused by 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC), and HDL uptake and disassembly due to the decreased binding to the LDL receptor.