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| 1 | Epigenetic regulation in alcoholic liver disease显示文摘Alcoholic liver disease(ALD)is characterized by steatosis or fat deposition in the liver and inflammation,which leads to cirrhosis and hepatocellular carcinoma.Induction of target genes without involving changes in DNA sequence seems to contribute greatly to liver injury. Chromatin modifications including alterations in histones and DNA,as well as post-transcriptional changes collectively referred to as epigenetic effects are altered by alcohol.Recent studies have pointed to a significant role for epigenetic mechanisms at the nucleosomal level influencing gene expression and disease outcome in ALD. Specifically,epigenetic alterations by alcohol include histone modifications such as changes in acetylation and phosphorylation,hypomethylation of DNA,and alterations in miRNAs.These modifications can be induced by alcoholinduced oxidative stress that results in altered recruitment of transcriptional machinery and abnormal gene expression.Delineating these mechanisms in initiation and progression of ALD is becoming a major area of interest.This review summarizes key epigenetic mechanisms that are dysregulated by alcohol in the liver.Alterations by alcohol in histone and DNA modifications,enzymes related to histone acetylation suchas histone acetyltransferases,histone deacetylases and sirtuins,and methylation enzymes such as DNA methyltransferases are discussed.Chromatin modifications and miRNA alterations that result in immune cell dysfunction contributing to inflammatory cytokine production in ALD is reviewed.Finally,the role of alcohol-mediated oxidative stress in epigenetic regulation in ALD is described. A better understanding of these mechanisms is crucial for designing novel epigenetic based therapies to ameliorate ALD. | Pranoti Mandrekar | 2011 | World Journal of Gastroenterology2011，17，20： | 10 |
| 2 | Signaling mechanisms in alcoholic liver injury: Role of transcription factors, kinases and heat shock proteins显示文摘Alcoholic liver injury comprises of interactions of various intracellular signaling events in the liver. Innate immune responses in the resident Kupffer cells of the liver, oxidative stress-induced activation of hepatocytes, fibrotic events in liver stellate cells and activation of liver sinusoidal endothelial cells all contribute to alcoholic liver injury. The signaling mechanisms associated with alcoholic liver injury vary based on the cell type involved and the extent of alcohol consumption. In this review we will elucidate the oxidative stress and signaling pathways affected by alcohol in hepatocytes and Kupffer cells in the liver by alcohol. The toll-like receptors and their down-stream signaling events that play an important role in alcohol-induced inflammation will be discussed. Alcohol-induced alterations of various intracellular transcription factors such as NFκB, PPARs and AP-1, as well as MAPK kinases in hepatocytes and macrophages leading to induction of target genes that contribute to liver injury will be reviewed. Finally, we will discuss the significance of heat shock proteins as chaperones and their functional regulation in the liver that could provide new mechanistic insights into the contributions of stress-induced signaling mechanisms in alcoholic liver injury. | Pranoti Mandrekar | 2007 | World Journal of Gastroenterology2007，13，37： | 3 |
| 3 | Signalling pathways in alcohol-induced liver inflammation<.--'Review' -->显示文摘 | Pranoti Mandrekar Gyongyi Szabo | 2009 | Journal of Hepatology2009，，6： | 2 |
| 4 | Signalling pathways in alcohol-induced liver inflammation<!--'Review' -->显示文摘 | Pranoti Mandrekar Gyongyi Szabo | 2009 | Journal of Hepatology2009，，6： | 2 |
| 5 | FOCUS ON: ALCOHOL AND THE LIVER显示文摘 | Szabo Gyongyi Mandrekar Pranoti | 2010 | Alcohol Research and Health (/)2010，，1： | 1 |
| 6 | An essential role for MCP-1 in alcoholic liver injury: regulation of pro-inflammatory cytokines and hepatic steatosis显示文摘 | Pranoti Mandrekar Aditya Ambade Arlene Lim | 2011 | Hepatology2011，54，6： | 1 |
| 7 | Signalling pathways in alcohol-induced liver inflammation<!--'Review' -->显示文摘 | Pranoti Mandrekar Gyongyi Szabo | 2009 | Journal of Hepatology2009，，6： | 1 |
| 8 | Innate Immune Response and Hepatic Inflammation显示文摘 | Gyongyi Szabo Pranoti Mandrekar Angela Dolganiuc | 2007 | Semin Liver Dis2007，，04： | 1 |
| 9 | Viral and Host Factors Induce Macrophage Activation and Loss of Toll-Like Receptor Tolerance in Chronic HCV Infection显示文摘 | Angela Dolganiuc Oxana Norkina Karen Kodys Donna Catalano Gennadiy Bakis Christopher Marshall Pranoti Mandrekar Gyongyi Szabo | 2007 | Gastroenterology2007，，5： | 1 |
| 10 | Pharmacological Inhibition of Heat Shock Protein 90 Alleviates Steatosis and Macrophage Activation in Murine Acute and Chronic Alcoholic Liver Injury显示文摘 | Aditya Ambade Donna Catalano Arlene Lim Andre Kopoyan Scott A. Shaffer Pranoti Mandrekar | 2014 | Journal of Hepatology2014，，： | 1 |
| 11 | Critical role of Toll-like receptors and the common TLR adaptor, MyD88, in induction of granulomas and liver injury显示文摘 | Arumugam Velayudham Istvan Hritz Angela Dolganiuc Pranoti Mandrekar Evelyn Kurt-Jones Gyongyi Szabo | 2006 | Journal of Hepatology2006，，6： | 1 |
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