<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhou X</submitter><funding>Key Technologies Research and Development Program</funding><funding>Jiangsu Province Capability Improvement Project through Science, Technology</funding><funding>Special Foundation for Science and Technology of Jiangsu Province</funding><pagination>e1013403</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12349724</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(8)</volume><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 </pubmed_abstract><journal>PLoS pathogens</journal><pubmed_title>A novel combination therapy with Uridine and Praziquantel effectively alleviates schistosomiasis-induced hepatic fibrosis through promoting adipogenic differentiation.</pubmed_title><pmcid>PMC12349724</pmcid><funding_grant_id>ZDXYS202207</funding_grant_id><funding_grant_id>2024YFC2310902</funding_grant_id><funding_grant_id>BZ2024044</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Xue Q</pubmed_authors><pubmed_authors>Wu C</pubmed_authors><pubmed_authors>Xiong C</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Zhou X</pubmed_authors><pubmed_authors>Dai Y</pubmed_authors><pubmed_authors>Xu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>A novel combination therapy with Uridine and Praziquantel effectively alleviates schistosomiasis-induced hepatic fibrosis through promoting adipogenic differentiation.</name><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 </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Aug</publication><modification>2026-04-07T18:32:22.987Z</modification><creation>2026-04-07T16:36:05.68Z</creation></dates><accession>S-EPMC12349724</accession><cross_references><pubmed>40768528</pubmed><doi>10.1371/journal.ppat.1013403</doi></cross_references></HashMap>