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. 2020 Jan 24;9(3):e014873. doi: 10.1161/JAHA.119.014873

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© 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Pathogenesis of endothelial damage attributable to HIV infection and its treatment: Viral proteins, inflammatory cytokines, and cART all lead to increase in reactive oxygen species (ROS). Oxidative stress induces endothelial nitic oxide synthase (eNOS) uncoupling leading to decreased nitric oxide (NO) availability. These events trigger endothelial dysfunction which is an important early step in endovascular damage and atherogenesis. This figure was created using http://www.biorender.com software. cART indicates combination antiretroviral therapy; IL‐1β, interleukin‐1 beta; IL‐16, interleukin‐16; Jak‐inh, Janus kinase inhibitor.