<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(6)</volume><submitter>Choi YY</submitter><pubmed_abstract>The accelerated course of hepatic fibrosis that occurs in some patients after liver transplantation is an important clinical problem. Activation of hepatic stellate cell (HSCs) is the dominant event in hepatic fibrosis. Previous studies have shown that treatment with mammalian target of rapamycin (mTOR) inhibitors was more effective in reducing the progression of fibrosis than treatment with calcineurin inhibitors, suggesting that mTOR could be a crucial target for inhibition of fibrosis. In addition, N-acetylcysteine (NAC) has been shown to effectively suppress HSC activation-dependent expression of alpha-smooth muscle actin in HSCs, suggesting that NAC could be a candidate for the clinical treatment of hepatic fibrosis. Here, we have evaluated the effects of immunosuppressive drugs and N</pubmed_abstract><journal>American journal of translational research</journal><pagination>2627-2639</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7344068</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Co-administration of everolimus and N-acetylcysteine attenuates hepatic stellate cell activation and hepatic fibrosis.</pubmed_title><pmcid>PMC7344068</pmcid><pubmed_authors>Choi YY</pubmed_authors><pubmed_authors>Kim DS</pubmed_authors><pubmed_authors>Hwang JI</pubmed_authors><pubmed_authors>Seok JI</pubmed_authors></additional><is_claimable>false</is_claimable><name>Co-administration of everolimus and N-acetylcysteine attenuates hepatic stellate cell activation and hepatic fibrosis.</name><description>The accelerated course of hepatic fibrosis that occurs in some patients after liver transplantation is an important clinical problem. Activation of hepatic stellate cell (HSCs) is the dominant event in hepatic fibrosis. Previous studies have shown that treatment with mammalian target of rapamycin (mTOR) inhibitors was more effective in reducing the progression of fibrosis than treatment with calcineurin inhibitors, suggesting that mTOR could be a crucial target for inhibition of fibrosis. In addition, N-acetylcysteine (NAC) has been shown to effectively suppress HSC activation-dependent expression of alpha-smooth muscle actin in HSCs, suggesting that NAC could be a candidate for the clinical treatment of hepatic fibrosis. Here, we have evaluated the effects of immunosuppressive drugs and N</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2025-04-19T18:00:51.495Z</modification><creation>2025-04-19T18:00:51.495Z</creation></dates><accession>S-EPMC7344068</accession><cross_references><pubmed>32655795</pubmed></cross_references></HashMap>