scholarly journals Ethanol metabolism and oxidative stress are required for unfolded protein response activation and steatosis in zebrafish with alcoholic liver disease

2013 ◽  
Vol 6 (5) ◽  
pp. 1213-1226 ◽  
Author(s):  
O. Tsedensodnom ◽  
A. M. Vacaru ◽  
D. L. Howarth ◽  
C. Yin ◽  
K. C. Sadler
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Unfolded Protein Response ◽  
Alcoholic Liver Disease ◽  
Ethanol Metabolism ◽  
Unfolded Protein ◽  
Protein Response ◽  
And Oxidative Stress ◽  
Response Activation

scholarly journals PERK-Mediated Unfolded Protein Response Activation and Oxidative Stress in PARK20 Fibroblasts

2019 ◽  
Vol 13 ◽  
Author(s):  
Giuseppina Amodio ◽  
Ornella Moltedo ◽  
Dominga Fasano ◽  
Lucrezia Zerillo ◽  
Marco Oliveti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Unfolded Protein Response ◽  
Unfolded Protein ◽  
Protein Response ◽  
And Oxidative Stress ◽  
Response Activation

scholarly journals Ursodeoxycholic acid: Effects on hepatic unfolded protein response, apoptosis and oxidative stress in morbidly obese patients

2017 ◽  
Vol 38 (3) ◽  
pp. 523-531 ◽  
Author(s):  
Michaela Mueller ◽  
Rui E. Castro ◽  
Anders Thorell ◽  
Hanns-Ulrich Marschall ◽  
Nicole Auer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ursodeoxycholic Acid ◽  
Unfolded Protein Response ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Unfolded Protein ◽  
Protein Response ◽  
And Oxidative Stress

Causal role of oxidative stress in unfolded protein response development in the hyperthyroid state

2015 ◽  
Vol 89 ◽  
pp. 401-408 ◽  
Author(s):  
Luis A. Videla ◽  
Virginia Fernández ◽  
Pamela Cornejo ◽  
Romina Vargas ◽  
Juan Carrasco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Unfolded Protein Response ◽  
Causal Role ◽  
Unfolded Protein ◽  
Hyperthyroid State ◽  
Protein Response

Unfolded protein response activation contributes to chemoresistance in hepatocellular carcinoma

2010 ◽  
Vol 22 (9) ◽  
pp. 1099-1105 ◽  
Author(s):  
Feras Y. Al-Rawashdeh ◽  
Peter Scriven ◽  
Ian C. Cameron ◽  
Patricia V. Vergani ◽  
Lynda Wyld
Keyword(s):  
Hepatocellular Carcinoma ◽  
Unfolded Protein Response ◽  
Unfolded Protein ◽  
Protein Response ◽  
Response Activation

scholarly journals Investigating RNA expression profiles altered by nicotinamide mononucleotide therapy in a chronic model of alcoholic liver disease

2019 ◽  
Vol 13 (1) ◽  
Author(s):  
Mohammed A. Assiri ◽  
Hadi R. Ali ◽  
John O. Marentette ◽  
Youngho Yun ◽  
Juan Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Mapk Pathway ◽  
Early Stage ◽  
Expression Profiles ◽  
Ethanol Metabolism ◽  
Metabolic Dysregulation ◽  
Nicotinamide Mononucleotide ◽  
The Impact

Abstract Background Chronic alcohol consumption is a significant cause of liver disease worldwide. Several biochemical mechanisms have been linked to the initiation and progression of alcoholic liver disease (ALD) such as oxidative stress, inflammation, and metabolic dysregulation, including the disruption of NAD+/NADH. Indeed, an ethanol-mediated reduction in hepatic NAD+ levels is thought to be one factor underlying ethanol-induced steatosis, oxidative stress, steatohepatitis, insulin resistance, and inhibition of gluconeogenesis. Therefore, we applied a NAD+ boosting supplement to investigate alterations in the pathogenesis of early-stage ALD. Methods To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice. Numerous strategies were employed to characterize the effect of NMN therapy, including the integration of RNA-seq, immunoblotting, and metabolomics analysis. Results Our findings reveal that NMN therapy increased hepatic NAD+ levels, prevented an ethanol-induced increase in plasma ALT and AST, and changed the expression of 25% of the genes that were modulated by ethanol metabolism. These genes were associated with a number of pathways including the MAPK pathway. Interestingly, our analysis revealed that NMN treatment normalized Erk1/2 signaling and prevented an induction of Atf3 overexpression. Conclusions These findings reveal previously unreported mechanisms by which NMN supplementation alters hepatic gene expression and protein pathways to impact ethanol hepatotoxicity in an early-stage murine model of ALD. Overall, our data suggest further research is needed to fully characterize treatment paradigms and biochemical implications of NAD+-based interventions.

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