Filtered By:
Condition: Liver Disease

This page shows you your search results in order of relevance. This is page number 2.

Order by Relevance | Date

Total 328 results found since Jan 2013.

RNAi Therapeutics for Diseases Involving Protein Aggregation: Fazirsiran for Alpha-1 Antitrypsin Deficiency-associated Liver Disease
This article describes the role of misfolded proteins and protein aggregates in disease, and options for therapeutic approaches. The RNAi mechanism is discussed, along with how the siRNA therapeutic fazirsiran for the treatment of AATD was developed. We also describe implications of siRNA therapeutics in extrahepatic diseases.EXPERT OPINION: Using RNAi as a therapeutic approach is well suited to treat disease in conditions where an excess of a protein or the effect of an abnormal mutated protein causes disease. The results observed for the first few siRNA therapeutics that were approved or are in development provide an imp...
Source: Expert Opinion on Investigational Drugs - July 20, 2023 Category: Drugs & Pharmacology Authors: Pavel Strnad Javier San Martin Source Type: research

RNAi therapeutics for diseases involving protein aggregation: fazirsiran for alpha-1 antitrypsin deficiency-associated liver disease
This article describes the role of misfolded proteins and protein aggregates in disease and options for therapeutic approaches. The RNAi mechanism is discussed, along with how the siRNA therapeutic fazirsiran for the treatment of AATD was developed. We also describe the implications of siRNA therapeutics in extrahepatic diseases.EXPERT OPINION: Using RNAi as a therapeutic approach is well suited to treat disease in conditions where an excess of a protein or the effect of an abnormal mutated protein causes disease. The results observed for the first few siRNA therapeutics that were approved or are in development provide an ...
Source: Expert Opinion on Investigational Drugs - July 20, 2023 Category: Drugs & Pharmacology Authors: Pavel Strnad Javier San Martin Source Type: research

Abstract 3171: Overexpression of a cancer stem cell marker doublecortin-like kinase (DCLK1) leads to activation of inflammatory cascade during development of virus-induced hepatocellular carcinoma
Conclusions: DCLK1 overexpression appears to be intimately related to the activation of pro-inflammatory and MAPK signaling pathways during the development of virus-induced pre-neoplastic conditions and initiation of tumors in liver. Thus, targeting DCLK1 at early stage of liver diseases may prevent virus-induced cirrhosis and HCC. Citation Format: Naushad Ali, Parthasarathy Chandrakesan, Mark Huycke, Sanam Husain, Allison F. Gillaspy, Randal May, William L. Berry, Sripathi Sureban, Dongfeng Qu, Nathaniel Weygant, Michael S. Bronze, Danny N. Dhanasekaran, Courtney W. Houchen. Overexpression of a cancer stem cell marker dou...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Ali, N., Chandrakesan, P., Huycke, M., Husain, S., Gillaspy, A. F., May, R., Berry, W. L., Sureban, S., Qu, D., Weygant, N., Bronze, M. S., Dhanasekaran, D. N., Houchen, C. W. Tags: Carcinogenesis Source Type: research

Glucagon‐like peptide‐1 (GLP‐1) preserves non‐alcoholic fatty liver disease (NAFLD) through inhibition of the endoplasmic reticulum (ER) stress‐associated pathway
ConclusionGLP‐1 protected against non‐alcoholic fatty liver disease by inactivating the ER stress‐associated apoptosis pathway. In addition, the effect was possibly related to the signaling pathway of ERp46. This article is protected by copyright. All rights reserved.
Source: Hepatology Research - July 4, 2015 Category: Internal Medicine Authors: Na. Ao, Jing Yang, Xiaochen Wang, Jian Du Tags: Original Article Source Type: research

Glucagon‐like peptide‐1 preserves non‐alcoholic fatty liver disease through inhibition of the endoplasmic reticulum stress‐associated pathway
ConclusionGLP‐1 protected against NAFLD by inactivating the ER stress‐associated apoptosis pathway. In addition, the effect was possibly related to the signaling pathway of ERp46.
Source: Hepatology Research - August 18, 2015 Category: Internal Medicine Authors: Na Ao, Jing Yang, Xiaochen Wang, Jian Du Tags: Original Article Source Type: research

Inhibition of citrate cotransporter Slc13a5/mINDY by RNAi improves hepatic insulin sensitivity and prevents diet-induced non-alcoholic fatty liver disease in mice
Conclusions We show that inducible mINDY inhibition improved hepatic insulin sensitivity and prevented diet-induced non-alcoholic fatty liver disease in adult C57BL6/J mice. These effects did not depend on changes of body weight or body composition. Graphical abstract
Source: Molecular Metabolism - August 13, 2016 Category: Endocrinology Source Type: research

PKC δ Silencing Alleviates Saturated Fatty Acid-Induced ER Stress by Enhancing SERCA Activity.
Conclusion : To the best of our knowledge, this is the first report demonstrating that the inhibition of PKCδ alleviates ERS by enhancing SERCA activity and stabilizing calcium homeostasis. PMID: 29046367 [PubMed - as supplied by publisher]
Source: Bioscience Reports - October 18, 2017 Category: Biomedical Science Authors: Lai S, Li Y, Kuang Y, Cui H, Yang Y, Sun W, Liu K, Chen D, Yan Q, Wen L Tags: Biosci Rep Source Type: research

Cytochrome P450 1A1 (CYP1A1) Catalyzes Lipid Peroxidation of Oleic Acid-Induced HepG2 Cells
AbstractNonalcoholic fatty liver disease (NAFLD) is a chronic hepatic disease associated with excessive accumulation of lipids in hepatocytes. As the disease progresses, oxidative stress plays a pivotal role in the development of hepatic lipid peroxidation. Cytochrome P450 1A1 (CYP1A1), a subtype of the cytochrome P450 family, has been shown to be a vital modulator in production of reactive oxygen species. However, the exact role of CYP1A1 in NAFLD is still unclear. The aim of this study was to investigate the effects of CYP1A1 on lipid peroxidation in oleic acid (OA)-treated human hepatoma cells (HepG2). We found that the...
Source: Biochemistry (Moscow) - May 1, 2018 Category: Biochemistry Source Type: research

Effect of celastrol on toll ‑like receptor 4‑mediated inflammatory response in free fatty acid‑induced HepG2 cells.
Effect of celastrol on toll‑like receptor 4‑mediated inflammatory response in free fatty acid‑induced HepG2 cells. Int J Mol Med. 2018 Jul 12;: Authors: Han LP, Sun B, Li CJ, Xie Y, Chen LM Abstract Toll‑like receptor 4 (TLR4)‑mediated immune and inflammatory signaling serves a pivotal role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study demonstrated that celastrol treatment was able to improve hepatic steatosis and inhibit the TLR4 signaling cascade pathway in type 2 diabetic rats. The present study aimed to investigate the effects of celastrol on trigly...
Source: International Journal of Molecular Medicine - July 12, 2018 Category: Molecular Biology Authors: Han LP, Sun B, Li CJ, Xie Y, Chen LM Tags: Int J Mol Med Source Type: research

CYP1A2 contributes to alcohol-induced abnormal lipid metabolism through the PTEN/AKT/SREBP-1c pathway.
In this study, we aimed to explore the role of CYP1A2 in lipid metabolism abnormalities induced by alcohol and to investigate the underlying mechanisms. L02 cells were treated with siRNA-CYP1A2 or fluvoxamine and then stimulated with 100 mM ethanol for 24 h. The levels of ALT and TGs in the siRNA-CYP1A2 and fluvoxamine groups were significantly lower than those in the normal control group after ethanol treatment, and the expression of SREBP-1c was decreased when CYP1A2 was inhibited, suggesting that CYP1A2 may contribute to alcohol-induced irregular lipid metabolism by regulating sterol regulatory element-binding prote...
Source: Biochemical and Biophysical Research communications - April 8, 2019 Category: Biochemistry Authors: Zhu Q, Huang C, Meng X, Li J Tags: Biochem Biophys Res Commun Source Type: research

Thymosin beta 4 alleviates non-alcoholic fatty liver by inhibiting ferroptosis via up-regulation of GPX4
This study revealed that Tβ4 protects hepatocytes by inhibiting the GPX4-mediated ferroptosis pathway, which provides a new strategy and target for the treatment of NAFLD.PMID:34280397 | DOI:10.1016/j.ejphar.2021.174351
Source: European Journal of Pharmacology - July 19, 2021 Category: Drugs & Pharmacology Authors: Zixin Zhu Ya Zhang Xinhao Huang Li Can Xueke Zhao Yinghui Wang Jing Xue Mingliang Cheng Lili Zhu Source Type: research