• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

GSE233807 RNA N6-methyladenosine methyltransferase METTL3 drives NAFLD-HCC and is a therapeutic target for boosting immunotherapy m6A-seq
Series Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensNon-alcoholic fatty liver disease (NAFLD) is an emerging risk factor of hepatocellular carcinoma (HCC). However, the mechanism and target therapy on NAFLD-HCC are still unclear. Here, we identify that the N6-methyladenosine (m6A) methyltransferase METTL3 promotes NAFLD-HCC. Hepatocyte-specific Mettl3 knockin exacerbated NAFLD-HCC formation while Mettl3 knockout exerted an opposite effect in mice. Single-cell RNA-seq revealed that METTL3 suppressed antitumor immune response by reducing infiltration of Gzmb+ and IFN- γ+ CD8+ T-cell, ther...
Source: GEO: Gene Expression Omnibus - August 23, 2023 Category: Genetics & Stem Cells Tags: Methylation profiling by high throughput sequencing Homo sapiens Source Type: research

GSE233806 RNA N6-methyladenosine methyltransferase METTL3 drives NAFLD-HCC and is a therapeutic target for boosting immunotherapy RNA-Seq
Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensNon-alcoholic fatty liver disease (NAFLD) is an emerging risk factor of hepatocellular carcinoma (HCC). However, the mechanism and target therapy on NAFLD-HCC are still unclear. Here, we identify that the N6-methyladenosine (m6A) methyltransferase METTL3 promotes NAFLD-HCC. Hepatocyte-specific Mettl3 knockin exacerbated NAFLD-HCC formation while Mettl3 knockout exerted an opposite effect in mice. Single-cell RNA-seq revealed that METTL3 suppressed antitumor immune response by reducing infiltration of Gzmb+ and IFN- γ+ CD8+ T-cell, there...
Source: GEO: Gene Expression Omnibus - August 23, 2023 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Source Type: research

Activation of the AMPK-SIRT1 pathway contributes to protective effects of Salvianolic acid A against lipotoxicity in hepatocytes and NAFLD in mice
Conclusion: Our data uncover a novel mechanism for hepatoprotective effects of Sal A against lipotoxicity both in livers from HFCD-fed mice and palmitic acid-treated hepatocytes.
Source: Frontiers in Pharmacology - November 30, 2020 Category: Drugs & Pharmacology Source Type: research

Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome. Ethics Statement This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

NF κB and Kidney Injury
Conclusion As a critical regulator of inflammation and cell survival, the NFκB pathway is a promising target for diagnosing and treating kidney diseases. For modulation of the NFκB pathway in the clinic, a number of molecules can effectively inhibit NFκB signaling by targeting the receptors, associated adaptors, IKKs, IκBs and transcriptional regulators (144). There is further clinical evidence on small-molecule inhibitors of IKKα and NIK from recent trials on anti-cancer therapies (145). These clinical trials showed that the cancer-selective pharmacodynamic response of DTP3, the co...
Source: Frontiers in Immunology - April 15, 2019 Category: Allergy & Immunology Source Type: research

ZNF300 stimulates fatty acid oxidation and alleviates hepatosteatosis through regulating PPAR{alpha}
ZNF300 plays an important role in the regulation of HBV-related hepatocellular carcinoma. However, little is known about the role of ZNF300 in lipid metabolism and NAFLD. In the present study, we observed that ZNF300 expression was markedly decreased in free fatty acid (FFA)-induced fatty liver. Overexpressed ZNF300 alleviated hepatic lipid accumulation, whereas knockdown of ZNF300 enhanced the FFA-induced lipid accumulation. Investigations of the underlying mechanisms revealed that ZNF300 directly binds to and regulates the PPARα expression, thus promoting fatty acid oxidation. Furthermore, bisulfite pyrosequencing ...
Source: Biochemical Journal - January 31, 2019 Category: Biochemistry Authors: Yan, F.-J., Wang, Y.-J., Yan, S.-R., Lu, J., Zheng, Y.-L. Tags: Research Articles Source Type: research

ZNF300 stimulates fatty acid oxidation and alleviates hepatosteatosis through regulating PPAR α.
ZNF300 stimulates fatty acid oxidation and alleviates hepatosteatosis through regulating PPARα. Biochem J. 2018 Dec 19;: Authors: Yan FJ, Wang YJ, Yan SR, Lu J, Zheng YL Abstract ZNF300 plays an important role in the regulation of HBV-related hepatocellular carcinoma. However, little is known about the role of ZNF300 in lipid metabolism and NAFLD. In the present study, we observed that ZNF300 expression was markedly decreased in free fatty acids (FFAs)-induced fatty liver. Overexpressed ZNF300 alleviated hepatic lipid accumulation, whereas knockdown of ZNF300 enhanced the FFAs-induced lipid accumulat...
Source: The Biochemical Journal - December 19, 2018 Category: Biochemistry Authors: Yan FJ, Wang YJ, Yan SR, Lu J, Zheng YL Tags: Biochem J Source Type: research

Repin1 deficiency in liver tissue alleviates NAFLD progression in mice
This study provides evidence that loss of Repin1 in the liver attenuates NAFLD progression, most likely by reducing fat accumulation and alleviating chronic tissue inflammation. Thus, modulating Repin1 expression may become a novel strategy and potential tool to inhibit NAFLD progression.Graphical abstract
Source: Journal of Advanced Research - November 23, 2018 Category: Research Source Type: research

A Novel Regulatory Role of Apoptosis Antagonizing Transcription Factor in the Pathogenesis of NAFLD and HCC
Conclusion AATF drives NAFLD and hepatocarcinogenesis, offering a potential target for therapeutic intervention.This article is protected by copyright. All rights reserved.
Source: Hepatology - November 5, 2018 Category: Internal Medicine Authors: Divya P. Kumar, Prasanna K. Santhekadur, Mulugeta Seneshaw, Faridoddin Mirshahi, Cora Uram Tuculescu, Arun J. Sanyal Tags: Original Article 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

Omega-3 polyunsaturated fatty acids protect human hepatoma cells from developing steatosis through FFA4 (GPR120)
Publication date: Available online 7 November 2017 Source:Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids Author(s): Saeromi Kang, Jin Huang, Bo-Kyung Lee, Young-Suk Jung, Eunok Im, Jung-Min Koh, Dong-Soon Im Protective effect of omega-3 polyunsaturated fatty acids (n-3 PUFA) on non-alcoholic fatty liver disease has been demonstrated. FFA4 (also known as GPR120; a G protein-coupled receptor) has been suggested to be a target of n-3 PUFA. FFA4 expression in hepatocytes has also been reported from liver biopsies in child fatty liver patients. In order to assess the functional role of FFA4 in hepat...
Source: Biochimica et Biophysica Acta (BBA) Molecular and Cell Biology of Lipids - November 8, 2017 Category: Lipidology Source Type: research

Omega-3 polyunsaturated fatty acids protect human hepatoma cells from developing steatosis through FFA4 (GPR120).
Abstract Protective effect of omega-3 polyunsaturated fatty acids (n-3 PUFA) on non-alcoholic fatty liver disease has been demonstrated. FFA4 (also known as GPR120; a G protein-coupled receptor) has been suggested to be a target of n-3 PUFA. FFA4 expression in hepatocytes has also been reported from liver biopsies in child fatty liver patients. In order to assess the functional role of FFA4 in hepatic steatosis, we used an in vitro model of liver X receptor (LXR)-mediated hepatocellular steatosis. FFA4 expression was confirmed in Hep3B and HepG2 human hepatoma cells. T0901317 (a specific LXR activator) induced lip...
Source: Biochimica et Biophysica Acta - November 7, 2017 Category: Biochemistry Authors: Kang S, Huang J, Lee BK, Jung YS, Im E, Koh JM, Im DS Tags: Biochim Biophys Acta Source Type: research

Apelin protects against liver X receptor-mediated steatosis through AMPK and PPAR α in human and mouse hepatocytes.
Apelin protects against liver X receptor-mediated steatosis through AMPK and PPARα in human and mouse hepatocytes. Cell Signal. 2017 Aug 15;39:84-94 Authors: Huang J, Kang S, Park SJ, Im DS Abstract Non-alcoholic fatty liver disease is the most commonly occurring chronic liver disease, and hepatic steatosis, a condition defined as extensive lipid accumulation in hepatocytes, is associated with liver dysfunction and metabolic diseases, such as, obesity and type II diabetes. Apelin is an adipokine that acts on a G protein-coupled receptor named APJ, and has been established to play pivotal roles in var...
Source: Cellular Signalling - August 15, 2017 Category: Cytology Authors: Huang J, Kang S, Park SJ, Im DS Tags: Cell Signal Source Type: research

RNA Interference as a Therapeutic Strategy for the Treatment of Liver Diseases.
Abstract RNA interference has emerged as an innovative technology for gene silencing that degrades mRNAs complementary to the antisense strands of double-stranded, short interfering RNAs (siRNAs). Its therapeutic application has important advantages over small-molecule drugs since offers the possibility of targeting virtually all genes and allows selective silencing of one or several genes. So far, a relative small proportion of cellular proteins can bind and respond to chemical drugs. Based on that, RNA interference-mediated gene silencing is widely considered as a crucial breakthrough in molecular biology with a...
Source: Current Pharmaceutical Design - October 23, 2015 Category: Drugs & Pharmacology Authors: Gonzalez-Rodriguez A, Valverde AM Tags: Curr Pharm Des Source Type: research

Metabolic profiling reveals that PNPLA3 induces widespread effects on metabolism beyond triacylglycerol remodeling in Huh-7 hepatoma cells
PNPLA3 was recently associated with the susceptibility to nonalcoholic fatty liver disease, a common cause of chronic liver disease characterized by abnormal triglyceride accumulation. Although it is established that PNPLA3 has both triacylglycerol lipase and acylglycerol O-acyltransferase activities, is still unknown whether the gene has any additional role in the modulation of the human liver metabolome. To uncover the functional role of PNPLA3 on liver metabolism, we performed high-throughput metabolic profiling of PNPLA3 siRNA-silencing and overexpression of wild-type and mutant Ile148Met variants (isoleucine/methionin...
Source: AJP: Gastrointestinal and Liver Physiology - July 1, 2014 Category: Gastroenterology Authors: Min, H.-K., Sookoian, S., Pirola, C. J., Cheng, J., Mirshahi, F., Sanyal, A. J. Tags: LIVER AND BILIARY TRACT Source Type: research

Pages: 1  2