<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>27(5)</volume><submitter>Li Y</submitter><pubmed_abstract>High salt can induce cardiac damage. The aim of this present study was to explore the effect and the mechanism of microRNA (miR)-142-3p on the cardiac fibrosis induced by high salt. Rats received high salt diet to induce cardiac fibrosis &lt;i>in vivo&lt;/i>, and neonatal rat cardiac fibroblasts (NRCF) treated with sodium chloride (NaCl) to induce fibrosis &lt;i>in vitro&lt;/i>. The fibrosis and mitochondrial autophagy levels were increased the heart and NRCF treated with NaCl, which were alleviated by miR-142-3p upregulation. The fibrosis and mitochondrial autophagy levels were elevated in NRCF after treating with miR-142-3p antagomiR. Optineurin (OPTN) expression was increased in the mitochondria of NRCF induced by NaCl, which was attenuated by miR-142-3p agomiR. OPTN downregulation inhibited the in</pubmed_abstract><journal>iScience</journal><pagination>109764</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11079474</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MicroRNA-142-3p alleviated high salt-induced cardiac fibrosis via downregulating optineurin-mediated mitophagy.</pubmed_title><pmcid>PMC11079474</pmcid><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Hu Y</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Zhao K</pubmed_authors><pubmed_authors>Yang F</pubmed_authors></additional><is_claimable>false</is_claimable><name>MicroRNA-142-3p alleviated high salt-induced cardiac fibrosis via downregulating optineurin-mediated mitophagy.</name><description>High salt can induce cardiac damage. The aim of this present study was to explore the effect and the mechanism of microRNA (miR)-142-3p on the cardiac fibrosis induced by high salt. Rats received high salt diet to induce cardiac fibrosis &lt;i>in vivo&lt;/i>, and neonatal rat cardiac fibroblasts (NRCF) treated with sodium chloride (NaCl) to induce fibrosis &lt;i>in vitro&lt;/i>. The fibrosis and mitochondrial autophagy levels were increased the heart and NRCF treated with NaCl, which were alleviated by miR-142-3p upregulation. The fibrosis and mitochondrial autophagy levels were elevated in NRCF after treating with miR-142-3p antagomiR. Optineurin (OPTN) expression was increased in the mitochondria of NRCF induced by NaCl, which was attenuated by miR-142-3p agomiR. OPTN downregulation inhibited the in</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 May</publication><modification>2026-06-01T05:25:37.5Z</modification><creation>2026-04-08T09:33:25.064Z</creation></dates><accession>S-EPMC11079474</accession><cross_references><pubmed>38726368</pubmed><doi>10.1016/j.isci.2024.109764</doi></cross_references></HashMap>