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. 2021 Jun 16;14(6):573. doi: 10.3390/ph14060573

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© 2021 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 (https://creativecommons.org/licenses/by/4.0/).

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NRF2 signaling and inflammation. Under basal conditions, NRF2 is bound to its repressor, KEAP1 and ultimately degraded by the proteasome following ubiquitination. However, under oxidative stress, free NRF2 translocates to the nucleus and dimerizes with small MAF family proteins. This complex binds to and promotes the expression of genes with an antioxidant response element, such as HO-1. HO-1 directly inhibits pro-inflammatory cytokines while upregulating anti-inflammatory cytokines as well as catalyzing the breakdown of heme into carbon monoxide, free iron, and biliverdin. Carbon monoxide is an inhibitor of the NFκB pathway, resulting in an overall decrease of pro-inflammatory cytokines. The image in Figure 5 was created using BioRender.com.