[1] Bartke N, Hannun YA. Bioactive sphingolipids: metabolism and function. J Lipid Res, 2009,50 Suppl:S91-6. [2] Lingwood D, Simons K. Lipid rafts as a membrane-organizing principle. Science, 2010,327: 46-50. [3] Hawkes DJ, Mak J. Lipid membrane; a novel target for viral and bacterial pathogens. Curr Drug Targets, 2006,7: 1615-1621. [4] Schneider-Schaulies J, Schneider-Schaulies S. Sphingolipids in viral infection. Biol Chem, 2014. [5] Dabrowska MM, Panasiuk A, Flisiak R. Signal transduction pathways in liver and the influence of hepatitis C virus infection on their activities. World J Gastroenterol, 2009,15: 2184-2189. [6] Roe B, Kensicki E, Mohney R, et al. Metabolomic profile of hepatitis C virus-infected hepatocytes. PLoS One, 2011,6: e23641. [7] Hirata Y, Ikeda K, Sudoh M, et al. Self-enhancement of hepatitis C virus replication by promotion of specific sphingolipid biosynthesis. PLoS Pathog, 2012,8: e1002860. [8] Weng L, Hirata Y, Arai M, et al. Sphingomyelin activates hepatitis C virus RNA polymerase in a genotype-specific manner. J Virol, 2010,84: 11761-11770. [9] Zhang JY, Qu F, Li JF, et al. Up-regulation of plasma hexosylceramide (d18: 1/18: 1) contributes to genotype 2 virus replication in chronic hepatitis C: a 20-year cohort study. Medicine (Baltimore), 2016,95: e3773. [10] Umehara T, Sudoh M, Yasui F, et al. Serine palmitoyl-transferase inhibitor suppresses HCV replication in a mouse model. Biochem Biophys Res Commun, 2006,346: 67-73. [11] Katsume A, Tokunaga Y, Hirata Y, et al. A serine palmitoyltransferase inhibitor blocks hepatitis C virus replication in human hepatocytes. Gastroenterology, 2013,145: 865-873. [12] Sakamoto H, Okamoto K, Aoki M, et al. Host sphingolipid biosynthesis as a target for hepatitis C virus therapy. Nat Chem Biol, 2005,1: 333-337. [13] Aizaki H, Morikawa K, Fukasawa M, et al. Critical role of virion-associated cholesterol and sphingolipid in hepatitis C virus infection. J Virol, 2008,82: 5715-5724. [14] Amako Y, Syed GH, Siddiqui A. Protein kinase D negatively regulates hepatitis C virus secretion through phosphorylation of oxysterol-binding protein and ceramide transfer protein. J Biol Chem, 2011,286: 11265-11274. [15] Haid S, Pietschmann T, Pecheur EI. Low pH-dependent hepatitis C virus membrane fusion depends on E2 integrity, target lipid composition, and density of virus particles. J Biol Chem, 2009,284: 17657-17667. [16] Voisset C, Lavie M, Helle F, et al. Ceramide enrichment of the plasma membrane induces CD81 internalization and inhibits hepatitis C virus entry. Cell Microbiol, 2008,10: 606-617. [17] Mari M, Fernandez-Checa JC. Sphingolipid signalling and liver diseases. Liver Int, 2007,27: 440-450. [18] Grammatikos G, Muhle C, Ferreiros N, et al. Serum acid sphingomyelinase is upregulated in chronic hepatitis C infection and non alcoholic fatty liver disease. Biochim Biophys Acta, 2014,1841: 1012-1020. [19] Li JF, Qu F, Zheng SJ, et al. Plasma sphingolipids as potential indicators of hepatic necroinflammation in patients with chronic hepatitis C and normal alanine aminotransferase level. PLoS One, 2014, 9: e95095. [20] Shea BS, Tager AM. Sphingolipid regulation of tissue fibrosis. Open Rheumatol J, 2012,6:123-129. [21] Li C, Zheng S, You H, et al. Sphingosine 1-phosphate (S1P)/S1P receptors are involved in human liver fibrosis by action on hepatic myofibroblasts motility. J Hepatol, 2011,54: 1205-1213. [22] Safadi R, Zigmond E, Pappo O, et al. Amelioration of hepatic fibrosis via beta-glucosylceramide-mediated immune modulation is associated with altered CD8 and NKT lymphocyte distribution. Int Immunol, 2007,19: 1021-1029. [23] Ikeda H, Ohkawa R, Watanabe N, et al. Plasma concentration of bioactive lipid mediator sphingosine 1-phosphate is reduced in patients with chronic hepatitis C. Clin Chim Acta, 2010,411: 765-770. [24] Li JF, Qu F, Zheng SJ, et al. Plasma sphingolipids: potential biomarkers for severe hepatic fibrosis in chronic hepatitis C. Mol Med Rep, 2015,12: 323-330. [25] Grammatikos G, Ferreiros N, Bon D, et al. Variations in serum sphingolipid levels associate with liver fibrosis progression and poor treatment outcome in HCV but not HBV infection. Hepatology, 2015, 61: 812-822. [26] Bijl N, Sokolovic M, Vrins C, et al. Modulation of glycosphingolipid metabolism significantly improves hepatic insulin sensitivity and reverses hepatic steatosis in mice. Hepatology, 2009,50:1431-1441. [27] Zhao H, Przybylska M, Wu IH, et al. Inhibiting glycosphingolipid synthesis ameliorates hepatic steatosis in obese mice. Hepatology, 2009,50: 85-93. [28] Yew NS, Zhao H, Hong EG, et al. Increased hepatic insulin action in diet-induced obese mice following inhibition of glucosylceramide synthase. PLoS One, 2010,5: e11239. [29] Jennemann R, Rothermel U, Wang S, et al. Hepatic glycosphingolipid deficiency and liver function in mice. Hepatology, 2010,51: 1799-1809. [30] Lombardo E, van Roomen CP, van Puijvelde GH, et al. Correction of liver steatosis by a hydrophobic iminosugar modulating glycosphingolipids metabolism. PLoS One, 2012, 7: e38520. [31] Bikman BT, Summers SA. Sphingolipids and hepatic steatosis. Adv Exp Med Biol, 2011,721:87-97. [32] Kurek K, Piotrowska DM, Wiesiolek-Kurek P, et al. Inhibition of ceramide de novo synthesis reduces liver lipid accumulation in rats with nonalcoholic fatty liver disease. Liver Int, 2014,34: 1074-1083. [33] Li JF, Qu F, Zheng SJ, et al. Elevated plasma sphingomyelin (d18:1/22:0) is closely related to hepatic steatosis in patients with chronic hepatitis C virus infection. Eur J Clin Microbiol Infect Dis, 2014,33: 1725-1732. [34] Tong M, Longato L, Ramirez T, et al. Therapeutic reversal of chronic alcohol-related steatohepatitis with the ceramide inhibitor myriocin. Int J Exp Pathol, 2014, 95: 49-63. [35] Li Y, Dong J, Ding T, et al. Sphingomyelin synthase 2 activity and liver steatosis: an effect of ceramide-mediated peroxisome proliferator-activated receptor gamma2 suppression. Arterioscler Thromb Vasc Biol, 2013, 33: 1513-1520. |