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. 2020 Nov 12;21(22):8533. doi: 10.3390/ijms21228533

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Upper panel: Proposed translational strategy for improved anti-inflammatory therapy using CD40–CD40L-antagonizing approaches. Lower panel: Key mechanisms of inflammation, atherothrombosis, oxidative stress and endothelial dysfunction. Improvement of these adverse key mechanisms by CD40(L)/TRAF inhibition. siRNA, small interfering RNA; ASOs, antisense oligonucleotides; TRAF-STOPs, inhibitors of TNF receptor associated factor; ECs, endothelial cells; VSMCs, vascular smooth muscle cells; NOX2, phagocytic NADPH oxidase (gp91phox); NOS2, inducible nitric oxide synthase; AGE, advanced glycation end products; RAGE, receptor for AGE; LDL, low density lipoprotein; WBC, white blood cell.

Upper panel: Proposed translational strategy for improved anti-inflammatory therapy using CD40–CD40L-antagonizing approaches. Lower panel: Key mechanisms of inflammation, atherothrombosis, oxidative stress and endothelial dysfunction. Improvement of these adverse key mechanisms by CD40(L)/TRAF inhibition. siRNA, small interfering RNA; ASOs, antisense oligonucleotides; TRAF-STOPs, inhibitors of TNF receptor associated factor; ECs, endothelial cells; VSMCs, vascular smooth muscle cells; NOX2, phagocytic NADPH oxidase (gp91phox); NOS2, inducible nitric oxide synthase; AGE, advanced glycation end products; RAGE, receptor for AGE; LDL, low density lipoprotein; WBC, white blood cell.