{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zakirova NF"],"funding":["111 Project","The DevWeCan French Laboratories of Excellence Network","Russian Science Foundation","ANRS-MIE","DevWeCan French Laboratories of Excellence Network"],"pagination":["1036"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11201506"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(12)"],"pubmed_abstract":["Hepatitis C virus (HCV) is an oncogenic virus that causes chronic liver disease in more than 80% of patients. During the last decade, efficient direct-acting antivirals were introduced into clinical practice. However, clearance of the virus does not reduce the risk of end-stage liver diseases to the level observed in patients who have never been infected. So, investigation of HCV pathogenesis is still warranted. Virus-induced changes in cell metabolism contribute to the development of HCV-associated liver pathologies. Here, we studied the impact of the virus on the metabolism of polyamines and proline as well as on the urea cycle, which plays a crucial role in liver function. It was found that HCV strongly suppresses the expression of arginase, a key enzyme of the urea cycle, leading to th"],"journal":["Cells"],"pubmed_title":["Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs the Urea Cycle."],"pmcid":["PMC11201506"],"funding_grant_id":["B12003","ANR-10-LABX-61","22157","19-74-10086"],"pubmed_authors":["Molle J","Valuev-Elliston VT","Smirnova OA","Ivanov AV","Zakirova NF","Bovet C","Grigorov B","Ivanova ON","Rindlisbacher B","Bartosch B","Karpenko IL","Khomutov AR","Monnier L","Yanvarev DV","Duponchel S","Khomich OA","Kochetkov SN","Golikov MV"],"additional_accession":[]},"is_claimable":false,"name":"Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs the Urea Cycle.","description":"Hepatitis C virus (HCV) is an oncogenic virus that causes chronic liver disease in more than 80% of patients. During the last decade, efficient direct-acting antivirals were introduced into clinical practice. However, clearance of the virus does not reduce the risk of end-stage liver diseases to the level observed in patients who have never been infected. So, investigation of HCV pathogenesis is still warranted. Virus-induced changes in cell metabolism contribute to the development of HCV-associated liver pathologies. Here, we studied the impact of the virus on the metabolism of polyamines and proline as well as on the urea cycle, which plays a crucial role in liver function. It was found that HCV strongly suppresses the expression of arginase, a key enzyme of the urea cycle, leading to th","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-04-08T19:06:29.629Z","creation":"2025-02-19T00:16:04.508Z"},"accession":"S-EPMC11201506","cross_references":{"pubmed":["38920664"],"doi":["10.3390/cells13121036"]}}