<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>Li P</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4>Sympathetic remodeling after myocardial infarction (MI) is the primary cause of ventricular arrhythmias (VAs), leading to sudden cardiac death (SCD). M1-type macrophages are closely associated with inflammation and sympathetic remodeling after MI. Long noncoding RNAs (lncRNAs) are critical for the regulation of cardiovascular disease development. Therefore, this study aimed to identify the lncRNAs involved in MI and reveal a possible regulatory mechanism.&lt;h4>Methods and results&lt;/h4>M0- and M1-type macrophages were selected for sequencing and screened for differentially expressed lncRNAs. The data revealed that lncRNA LOC100911717 was upregulated in M1-type macrophages but not in M0-type macrophages. In addition, the lncRNA LOC100911717 was upregulated in heart tissues aft</pubmed_abstract><journal>Frontiers in cardiovascular medicine</journal><pagination>1019435</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9859628</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats.</pubmed_title><pmcid>PMC9859628</pmcid><pubmed_authors>Qi L</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Yan S</pubmed_authors><pubmed_authors>Wang K</pubmed_authors><pubmed_authors>Shi Y</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Feng M</pubmed_authors><pubmed_authors>Ge W</pubmed_authors><pubmed_authors>Hu H</pubmed_authors><pubmed_authors>Lyu H</pubmed_authors><pubmed_authors>Yang P</pubmed_authors><pubmed_authors>Yin J</pubmed_authors></additional><is_claimable>false</is_claimable><name>lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats.</name><description>&lt;h4>Objective&lt;/h4>Sympathetic remodeling after myocardial infarction (MI) is the primary cause of ventricular arrhythmias (VAs), leading to sudden cardiac death (SCD). M1-type macrophages are closely associated with inflammation and sympathetic remodeling after MI. Long noncoding RNAs (lncRNAs) are critical for the regulation of cardiovascular disease development. Therefore, this study aimed to identify the lncRNAs involved in MI and reveal a possible regulatory mechanism.&lt;h4>Methods and results&lt;/h4>M0- and M1-type macrophages were selected for sequencing and screened for differentially expressed lncRNAs. The data revealed that lncRNA LOC100911717 was upregulated in M1-type macrophages but not in M0-type macrophages. In addition, the lncRNA LOC100911717 was upregulated in heart tissues aft</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-04-08T12:58:18.697Z</modification><creation>2025-02-19T03:00:07.384Z</creation></dates><accession>S-EPMC9859628</accession><cross_references><pubmed>36684596</pubmed><doi>10.3389/fcvm.2022.1019435</doi></cross_references></HashMap>