Signal transduction pathways in liver and the influence of hepatitis C virus infection on their activities.
In liver, the most intensively studied transmembrane and intracellular signal transduction pathways are the Janus kinase signal transduction pathway, the mitogen-activated protein kinases signal transduction pathway, the transforming growth factor beta signal transduction pathway, the tumor necrosis factor alpha signal transduction pathway and the recently discovered sphingolipid signal transduction pathway. All of them are activated by many different cytokines and growth factors. They regulate specific cell mechanisms such as hepatocytes proliferation, growth, differentiation, adhesion, apoptosis, and synthesis and degradation of the extracellular matrix. The replication cycle of hepatitis C virus (HCV) is intracellular and requires signal transduction to the nucleus to regulate transcription of its genes. Moreover, HCV itself, by its structural and non-structural proteins, could influence the activity of the second signal messengers. Thus, the inhibition of the transmembrane and intracellular signal transduction pathways could be a new therapeutic target in chronic hepatitis C treatment.
Department of Infectious Diseases and Hepatology, Medical University of Bialystok, 14 Zurawia Str, 15-540 Bialystok, Poland. m.dabrowska@op.pl
Magdalena-M
MM
Dabrowska
Anatol
A
Panasiuk
Robert
R
Flisiak
D016174:Hepacivirus / Q000378:metabolism*; D006526:Hepatitis C / Q000453:epidemiology / Q000503:physiopathology; D006801:Humans; D053612:Janus Kinases / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000821:virology; D008233:Lymphotoxin-alpha / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D013107:Sphingolipids / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D008233:Lymphotoxin-alpha; D013107:Sphingolipids; D014409:Tumor Necrosis Factor-alpha; D053612:Janus Kinases; D020928:Mitogen-Activated Protein Kinases