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Targeting N6-methyladenosine reader YTHDF1 with siRNA boosts antitumor immunity in NASH-HCC by inhibiting EZH2-IL-6 axis
RNA N6-methyladenosine (m6A) reader protein YTHDF1 has been implicated in cancer; however, its role in hepatocellular carcinoma (HCC), especially in non-alcoholic steatohepatitis-associated HCC (NASH-HCC), remains unknown. Here, we investigated the functional role of YTHDF1 in NASH-HCC and its interplay with the tumor immune microenvironment.
Source: Journal of Hepatology - July 15, 2023 Category: Gastroenterology Authors: Lina Wang, Lefan Zhu, Cong Liang, Xiang Huang, Ziqin Liu, Jihui Huo, Ying Zhang, Yifan Zhang, Lili Chen, Hongzhi Xu, Xiaoxing Li, Lixia Xu, Ming Kuang, Chi Chun Wong, Jun Yu Tags: Research Article Source Type: research

ATF4-mediated CD36 Upregulation Contributes to Palmitate-induced Lipotoxicity in Hepatocytes
In this study, our data revealed for the first time that ATF4 plays a critical role in mediating hepatic CD36 expression. Genetic inhibition of ATF4 attenuated CD36 upregulation induced by either palmitate or ER stress inducer tunicamycin in hepatocytes. In mice, tunicamycin upregulates liver CD36 expression, whereas hepatocyte-specific ATF4 knockout mice manifest lower hepatic CD36 expression when compared to control animals. Furthermore, we demonstrated that CD36 upregulation upon palmitate exposure represents a feedforward mechanism in that siRNA knockdown of CD36 in hepatocytes blunted ATF4 activation induced by both p...
Source: Am J Physiol Gastroi... - February 28, 2023 Category: Gastroenterology Authors: Alexandra Griffiths Jun Wang Qing Song Samuel Man Lee Jose Cordoba-Chacon Zhenyuan Song Source Type: research

MANF Protects Pancreatic Acinar Cells Against Alcohol ‐induced Endoplasmic Reticulum Stress and Cellular injury
ConclusionsMANF was protective against alcohol ‐induced ER stress and cellular injury in pancreatic acinar cells. The findings suggest a potential therapeutic value of MANF for alcoholic pancreatitis.
Source: Journal of Hepato-Biliary-Pancreatic Sciences - March 1, 2021 Category: Gastroenterology Authors: Huaxun Wu, Hui Li, Wen Wen, Yongchao Wang, Hong Xu, Mei Xu, Jacqueline A. Frank, Wei Wei, Jia Luo Tags: ORIGINAL ARTICLE Source Type: research

Folic acid attenuates high-fat diet-induced steatohepatitis via deacetylase SIRT1-dependent restoration of PPAR α.
CONCLUSION: Folic acid improves hepatic lipid metabolism by upregulating PPARα levels via a SIRT1-dependent mechanism and restores hepatic one-carbon metabolism and diversity of gut microbiota, thereby attenuating HFD-induced NASH in rats. PMID: 32476787 [PubMed - in process]
Source: World Journal of Gastroenterology : WJG - May 13, 2020 Category: Gastroenterology Authors: Xin FZ, Zhao ZH, Zhang RN, Pan Q, Gong ZZ, Sun C, Fan JG Tags: World J Gastroenterol Source Type: research

miR-192-5p regulates lipid synthesis in non-alcoholic fatty liver disease through SCD-1.
CONCLUSION: This study demonstrates that miR-192-5p has a negative regulatory role in lipid synthesis, which is mediated through its direct regulation of SCD-1. PMID: 29290651 [PubMed - in process]
Source: World Journal of Gastroenterology : WJG - December 14, 2017 Category: Gastroenterology Authors: Liu XL, Cao HX, Wang BC, Xin FZ, Zhang RN, Zhou D, Yang RX, Zhao ZH, Pan Q, Fan JG Tags: World J Gastroenterol Source Type: research

CD98 siRNA-loaded nanoparticles decrease hepatic steatosis in mice
Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid hepatic accumulation. Here, we investigated whether a reduction of CD98 expression mediated by CD98 siRNA-loaded nanoparticles (NPs) could attenuate liver disease markers in a mouse model of NAFLD. NPs were generated using a double emulsion/solvent evaporation technique. Mice fed a high fat diet for 8 weeks to induce fatty liver were treated with vein tail injections of CD98 siRNA-loaded NPs. In vitro, HepG2 treated with CD98 siRNA-loaded NPs showed significant downregulation of CD98 leading to a significant decrease of major pro-inflammatory cytokines and markers.
Source: Digestive and Liver Disease - November 16, 2016 Category: Gastroenterology Authors: Brandon S.B. Canup, Heliang Song, Vu Le Ngo, Xiangxiao Meng, Timothy L. Denning, Pallavi Garg, Hamed Laroui Tags: Liver, Pancreas and Biliary Tract Source Type: research

Osteopontin is an important mediator of alcoholic liver disease via hepatic stellate cell activation.
CONCLUSION: OPN is a key mediator of the alcohol-induced effects on hepatic stellate cell functions and liver fibrogenesis. PMID: 25278703 [PubMed - in process]
Source: World Journal of Gastroenterology : WJG - September 28, 2014 Category: Gastroenterology Authors: Seth D, Duly A, Kuo PC, McCaughan GW, Haber PS Tags: World J Gastroenterol Source Type: research

Apolipoprotein A‐I and adenosine triphosphate‐binding cassette transporter A1 expression alleviates lipid accumulation in hepatocytes
ConclusionsExpression of apoA‐I or ABCA1 can reduce steatosis by decreasing lipid storage in hepatocytes through lipid transport and may also reduce endoplasmic reticulum stress, further lessening hepatic steatosis.
Source: Journal of Gastroenterology and Hepatology - February 19, 2014 Category: Gastroenterology Authors: Wei Liu, Ling Qin, Hao Yu, Fangqiao Lv, Yutong Wang Tags: Hepatology Source Type: research

HMGB1 recruits hepatic stellate cells and liver endothelial cells to sites of ethanol-induced parenchymal cell injury
Hepatic stellate cells (HSC) and liver endothelial cells (LEC) migrate to sites of injury and perpetuate alcohol-induced liver injury. High-mobility group box 1 (HMGB1) is a protein released from the nucleus of injured cells that has been implicated as a proinflammatory mediator. We hypothesized that HMGB1 may be released from ethanol-stimulated liver parenchymal cells and contribute to HSC and LEC recruitment. Ethanol stimulation of rat hepatocytes and HepG2 cells resulted in translocation of HMGB1 from the nucleus as assessed by Western blot. HMGB1 protein levels were increased in the supernatant of ethanol-treated hepat...
Source: AJP: Gastrointestinal and Liver Physiology - December 5, 2013 Category: Gastroenterology Authors: Seo, Y. S., Kwon, J. H., Yaqoob, U., Yang, L., De Assuncao, T. M., Simonetto, D. A., Verma, V. K., Shah, V. H. Tags: INFLAMMATION/IMMUNITY/MEDIATORS Source Type: research

ApoA‐I and ABCA1 expression alleviates lipid accumulation in hepatocytes
ConclusionsExpression of apoA‐I or ABCA1 can reduce steatosis by decreasing lipid storage in hepatocytes through lipid transport and may also reduce ER stress, further lessening hepatic steatosis.
Source: Journal of Gastroenterology and Hepatology - November 13, 2013 Category: Gastroenterology Authors: Wei Liu, Ling Qin, Hao Yu, Fangqiao Lv, Yutong Wang Tags: Experimental Hepatology Source Type: research

HMGB1 recruits hepatic stellate cells and liver endothelial cells to sites of ethanol induced parenchymal cell injury.
Abstract Hepatic stellate cells (HSC) and liver endothelial cells (LEC) migrate to sites of injury and perpetuate alcohol induced liver injury. High mobility group box 1 (HMGB1) is a protein released from the nucleus of injured cells that has been implicated as a proinflammatory mediator. We hypothesized that HMGB1 may be released from ethanol-stimulated liver parenchymal cells and contribute to HSC and LEC recruitment. Ethanol stimulation of rat hepatocytes and HepG2 cells resulted in translocation of HMGB1 from the nucleus as assessed by Western blot. HMGB1 protein levels were increased in the supernatant of eth...
Source: Am J Physiol Gastroi... - October 3, 2013 Category: Gastroenterology Authors: Seo YS, Kwon JH, Yaqoob U, Yang L, de Assuncao TM, Simonetto DA, Verma VK, Shah VH Tags: Am J Physiol Gastrointest Liver Physiol Source Type: research

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