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. 2019 Jul 1;2019:8563845. doi: 10.1155/2019/8563845

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Copyright © 2019 Patricia Marchio et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Effects of oxLDL and oxidative stress on endothelium. LOX-1 activation by oxLDL induces endothelial oxidative stress by increasing NADPH oxidase (Nox) activity and uncoupling eNOS. Oxidative stress activates NF-κB through p38 mitogen-activated protein kinase (p38MAPK) and phosphatidylinositol 3-kinase (PI3K) transduction pathways initiating intranuclear apoptotic signal transduction. The formation of peroxynitrite (ONOO⁻) reduces nitric oxide (NO) and prostacyclin (PGI2) bioavailability leading to endothelial dysfunction. In addition, oxidative stress reduces PPARγ activity and adiponectin levels. Both of them stimulate AMP-activated protein kinase (AMPK) which in turn upregulates eNOS activity through Akt phosphorylation (Akt-P). Moreover, AMPK is a negative regulator of Nox.