<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>122(10)</volume><submitter>Zhang Y</submitter><pubmed_abstract>&lt;h4>Rationale&lt;/h4>Ca&lt;sup>2+&lt;/sup> homeostasis-a critical determinant of cardiac contractile function-is critically regulated by SERCA2a (sarcoplasmic reticulum Ca&lt;sup>2+&lt;/sup>-ATPase 2a). Our previous study has identified &lt;i>ZFAS1&lt;/i> as a new lncRNA biomarker of acute myocardial infarction (MI).&lt;h4>Objective&lt;/h4>To evaluate the effects of &lt;i>ZFAS1&lt;/i> on SERCA2a and the associated Ca&lt;sup>2+&lt;/sup> homeostasis and cardiac contractile function in the setting of MI.&lt;h4>Methods and results&lt;/h4>&lt;i>ZFAS1&lt;/i> expression was robustly increased in cytoplasm and sarcoplasmic reticulum in a mouse model of MI and a cellular model of hypoxia. Knockdown of endogenous &lt;i>ZFAS1&lt;/i> by virus-mediated silencing shRNA partially abrogated the ischemia-induced contractile dysfunction. Overexpression of &lt;i>ZFAS</pubmed_abstract><journal>Circulation research</journal><pagination>1354-1368</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5959220</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>LncRNA &lt;i>ZFAS1&lt;/i> as a SERCA2a Inhibitor to Cause Intracellular Ca&lt;sup>2+&lt;/sup> Overload and Contractile Dysfunction in a Mouse Model of Myocardial Infarction.</pubmed_title><pmcid>PMC5959220</pmcid><pubmed_authors>Jiao L</pubmed_authors><pubmed_authors>Pan Z</pubmed_authors><pubmed_authors>Li C</pubmed_authors><pubmed_authors>Lu Y</pubmed_authors><pubmed_authors>Xu C</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Yang B</pubmed_authors><pubmed_authors>Li M</pubmed_authors><pubmed_authors>Zhuang Y</pubmed_authors><pubmed_authors>Sun L</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Shao Y</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Gao Y</pubmed_authors><pubmed_authors>Yang R</pubmed_authors><pubmed_authors>Xuan L</pubmed_authors></additional><is_claimable>false</is_claimable><name>LncRNA &lt;i>ZFAS1&lt;/i> as a SERCA2a Inhibitor to Cause Intracellular Ca&lt;sup>2+&lt;/sup> Overload and Contractile Dysfunction in a Mouse Model of Myocardial Infarction.</name><description>&lt;h4>Rationale&lt;/h4>Ca&lt;sup>2+&lt;/sup> homeostasis-a critical determinant of cardiac contractile function-is critically regulated by SERCA2a (sarcoplasmic reticulum Ca&lt;sup>2+&lt;/sup>-ATPase 2a). Our previous study has identified &lt;i>ZFAS1&lt;/i> as a new lncRNA biomarker of acute myocardial infarction (MI).&lt;h4>Objective&lt;/h4>To evaluate the effects of &lt;i>ZFAS1&lt;/i> on SERCA2a and the associated Ca&lt;sup>2+&lt;/sup> homeostasis and cardiac contractile function in the setting of MI.&lt;h4>Methods and results&lt;/h4>&lt;i>ZFAS1&lt;/i> expression was robustly increased in cytoplasm and sarcoplasmic reticulum in a mouse model of MI and a cellular model of hypoxia. Knockdown of endogenous &lt;i>ZFAS1&lt;/i> by virus-mediated silencing shRNA partially abrogated the ischemia-induced contractile dysfunction. Overexpression of &lt;i>ZFAS</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 May</publication><modification>2026-06-14T06:12:37.481Z</modification><creation>2026-06-14T03:16:08.79Z</creation></dates><accession>S-EPMC5959220</accession><cross_references><pubmed>29475982</pubmed><doi>10.1161/CIRCRESAHA.117.312117</doi></cross_references></HashMap>