{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhou X"],"funding":["Key Technologies Research and Development Program","Jiangsu Province Capability Improvement Project through Science, Technology","Special Foundation for Science and Technology of Jiangsu Province"],"pagination":["e1013403"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12349724"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(8)"],"pubmed_abstract":["Schistosomiasis-induced hepatic fibrosis, a consequence of egg-induced granulomatous lesions, remains untreated by current drugs. Therefore, the development of novel antifibrosis drugs is of paramount importance. Our previous study indicated that aberrant uridine concentrations play a pivotal role in schistosomiasis-induced hepatic fibrosis. This study aimed to explore the inhibitory role of uridine in schistosomiasis-induced liver fibrosis and the regulatory mechanism of uridine on hepatic stellate cell (HSC) activation. The results indicated that uridine could inhibit schistosomiasis-induced liver fibrosis in vivo and TGF-β-induced HSC activation in vitro. Molecular docking revealed a strong interaction between uridine and the adenosine receptor A1 (ADORA1) receptor. Subsequent in vitro "],"journal":["PLoS pathogens"],"pubmed_title":["A novel combination therapy with Uridine and Praziquantel effectively alleviates schistosomiasis-induced hepatic fibrosis through promoting adipogenic differentiation."],"pmcid":["PMC12349724"],"funding_grant_id":["ZDXYS202207","2024YFC2310902","BZ2024044"],"pubmed_authors":["Liu X","Li X","Huang Y","Zhang Y","Xue Q","Wu C","Xiong C","Wang Y","Zhou X","Dai Y","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"A novel combination therapy with Uridine and Praziquantel effectively alleviates schistosomiasis-induced hepatic fibrosis through promoting adipogenic differentiation.","description":"Schistosomiasis-induced hepatic fibrosis, a consequence of egg-induced granulomatous lesions, remains untreated by current drugs. Therefore, the development of novel antifibrosis drugs is of paramount importance. Our previous study indicated that aberrant uridine concentrations play a pivotal role in schistosomiasis-induced hepatic fibrosis. This study aimed to explore the inhibitory role of uridine in schistosomiasis-induced liver fibrosis and the regulatory mechanism of uridine on hepatic stellate cell (HSC) activation. The results indicated that uridine could inhibit schistosomiasis-induced liver fibrosis in vivo and TGF-β-induced HSC activation in vitro. Molecular docking revealed a strong interaction between uridine and the adenosine receptor A1 (ADORA1) receptor. Subsequent in vitro ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-04-07T18:32:22.987Z","creation":"2026-04-07T16:36:05.68Z"},"accession":"S-EPMC12349724","cross_references":{"pubmed":["40768528"],"doi":["10.1371/journal.ppat.1013403"]}}