2020
DOI: 10.3390/cancers12102932
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Nrf2 in Neoplastic and Non-Neoplastic Liver Diseases

Abstract: Activation of the Keap1/Nrf2 pathway, the most important cell defense signal, triggered to neutralize the harmful effects of electrophilic and oxidative stress, plays a crucial role in cell survival. Therefore, its ability to attenuate acute and chronic liver damage, where oxidative stress represents the key player, is not surprising. On the other hand, while Nrf2 promotes proliferation in cancer cells, its role in non-neoplastic hepatocytes is a matter of debate. Another topic of uncertainty concerns the natu… Show more

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Cited by 15 publications
(13 citation statements)
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References 186 publications
(251 reference statements)
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“…In addition, as previously mentioned, PERK is responsible for regulating Nrf2 [ 41 ], which besides activating ABC transporter efflux pumps [ 39 ], has also been reported to promote anti-apoptotic signals [ 87 ]. The role of Nrf2 in blocking cell death was confirmed as inhibition of Nrf2 restored sensitivity to apoptosis and reversed chemoresistance in Bel-7402/5-FU cell lines [ 88 ].…”
Section: Mechanisms Of Drug Resistancementioning
confidence: 99%
“…In addition, as previously mentioned, PERK is responsible for regulating Nrf2 [ 41 ], which besides activating ABC transporter efflux pumps [ 39 ], has also been reported to promote anti-apoptotic signals [ 87 ]. The role of Nrf2 in blocking cell death was confirmed as inhibition of Nrf2 restored sensitivity to apoptosis and reversed chemoresistance in Bel-7402/5-FU cell lines [ 88 ].…”
Section: Mechanisms Of Drug Resistancementioning
confidence: 99%
“…Excessive accumulation of triglycerides in the liver will damage the mitochondrial respiratory chain. Liver is more susceptible to injury due to increased ROS, impaired antioxidant enzymes, and upregulated proinflammatory cytokines [128]. The main dietary factor contributing to NASH is increased consumption of refined carbohydrates and saturated fats [129].…”
Section: Diet In Non-alcoholic Steatohepatitis (Nash)mentioning
confidence: 99%
“…Thus, the electrophile oxidants could cause redox modification in the reactive cysteine residues, followed by the induction of conformational changes in Keap1, which subsequently impedes Nrf2 ubiquitination [ 96 , 97 ]. Thus, the nascent Nrf2 escapes from the Keap1-dependent degradation and undergoes translocation into nucleus to form heterodimers with sMAFs and binds to AREs or electrophilic-responsive elements of the promoter region of DNA to foster the transactivation of cytoprotective genes, viz., NAD(P)H:quinone oxidoreductase 1 (NQO1) of Phase I and heme oxygenase (HO)-1) of Phase II, glutathione S-transferase (GST), UDP-glucuronosyltransferase (UGT), and UDP-glucuronic acid (UGA) of Phase II and phase III enzymes [ 92 , 98 , 99 , 100 ]. Thus, during oxidative/electrophilic stress conditions, Nrf2/Keap1 launches several cytoprotective effects through the binding to the small MAF proteins [ 92 ].…”
Section: Nrf2 and Its Glycation And Deglycation Mechanisms In Regumentioning
confidence: 99%