<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen T</submitter><funding>Natural Science Foundation of Tianjin City</funding><funding>National Natural Science Foundation of China</funding><pagination>335</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9520944</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Long noncoding RNAs (lncRNAs) have emerged as important regulators in a variety of human diseases. The dysregulation of liver sinusoidal endothelial cell (LSEC) phenotype is a critical early event in the fibrotic process. However, the biological function of lncRNAs in LSEC still remains unclear.&lt;h4>Methods&lt;/h4>The expression level of lncRNA Airn was evaluated in both human fibrotic livers and serums, as well as mouse fibrotic livers. Gain- and loss-of-function experiments were performed to detect the effect of Airn on LSEC differentiation and hepatic stellate cell (HSC) activation in liver fibrosis. Furthermore, RIP, RNA pull-down-immunoblotting, and ChIP experiments were performed to explore the underlying mechanisms of Airn.&lt;h4>Results&lt;/h4>We have identified Airn was s</pubmed_abstract><journal>BMC medicine</journal><pubmed_title>LncRNA Airn maintains LSEC differentiation to alleviate liver fibrosis via the KLF2-eNOS-sGC pathway.</pubmed_title><pmcid>PMC9520944</pmcid><funding_grant_id>81971331</funding_grant_id><funding_grant_id>81870429</funding_grant_id><funding_grant_id>82170630</funding_grant_id><funding_grant_id>32171125</funding_grant_id><funding_grant_id>81800542</funding_grant_id><funding_grant_id>19JCZDJC36700</funding_grant_id><pubmed_authors>Zhang K</pubmed_authors><pubmed_authors>Hu Z</pubmed_authors><pubmed_authors>Han X</pubmed_authors><pubmed_authors>Du X</pubmed_authors><pubmed_authors>Yao Q</pubmed_authors><pubmed_authors>Shi Z</pubmed_authors><pubmed_authors>Han T</pubmed_authors><pubmed_authors>Zhao Y</pubmed_authors><pubmed_authors>Meng X</pubmed_authors><pubmed_authors>Zhao S</pubmed_authors><pubmed_authors>Zheng L</pubmed_authors><pubmed_authors>Lin H</pubmed_authors><pubmed_authors>Hong W</pubmed_authors><pubmed_authors>Chen T</pubmed_authors></additional><is_claimable>false</is_claimable><name>LncRNA Airn maintains LSEC differentiation to alleviate liver fibrosis via the KLF2-eNOS-sGC pathway.</name><description>&lt;h4>Background&lt;/h4>Long noncoding RNAs (lncRNAs) have emerged as important regulators in a variety of human diseases. The dysregulation of liver sinusoidal endothelial cell (LSEC) phenotype is a critical early event in the fibrotic process. However, the biological function of lncRNAs in LSEC still remains unclear.&lt;h4>Methods&lt;/h4>The expression level of lncRNA Airn was evaluated in both human fibrotic livers and serums, as well as mouse fibrotic livers. Gain- and loss-of-function experiments were performed to detect the effect of Airn on LSEC differentiation and hepatic stellate cell (HSC) activation in liver fibrosis. Furthermore, RIP, RNA pull-down-immunoblotting, and ChIP experiments were performed to explore the underlying mechanisms of Airn.&lt;h4>Results&lt;/h4>We have identified Airn was s</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2026-05-27T19:01:01.087Z</modification><creation>2025-02-19T01:55:45.916Z</creation></dates><accession>S-EPMC9520944</accession><cross_references><pubmed>36171606</pubmed><doi>10.1186/s12916-022-02523-w</doi></cross_references></HashMap>