<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Qi L</submitter><funding>China Postdoctoral Science Foundation</funding><funding>National Natural Science Foundation of China</funding><pagination>1264-1280</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8831944</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>26(4)</volume><pubmed_abstract>Ventricular arrhythmias (VAs) triggers by sympathetic nerve hyperactivity contribute to sudden cardiac death in myocardial infarction (MI) patients. Microglia-mediated inflammation in the paraventricular nucleus (PVN) is involved in sympathetic hyperactivity after MI. N6-methyladenosine (m&lt;sup>6&lt;/sup> A), the most prevalent mRNA and epigenetic modification, is critical for mediating cell inflammation. We aimed to explore whether METTL3-mediated m&lt;sup>6&lt;/sup> A modification is involved in microglia-mediated sympathetic hyperactivity after MI in the PVN. MI model was established by left coronary artery ligation. METTL3-mediated m&lt;sup>6&lt;/sup> A modification was markedly increased in the PVN at 3 days after MI, and METTL3 was primarily located in microglia by immunofluorescence. RNA-seq, MeRIP</pubmed_abstract><journal>Journal of cellular and molecular medicine</journal><pubmed_title>New insights into the central sympathetic hyperactivity post-myocardial infarction: Roles of METTL3-mediated m&lt;sup>6&lt;/sup> A methylation.</pubmed_title><pmcid>PMC8831944</pmcid><funding_grant_id>2016M602154</funding_grant_id><funding_grant_id>81870253</funding_grant_id><funding_grant_id>882070345</funding_grant_id><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>Zhao Y</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>Hu H</pubmed_authors><pubmed_authors>Lyu H</pubmed_authors><pubmed_authors>Xue M</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Yin J</pubmed_authors></additional><is_claimable>false</is_claimable><name>New insights into the central sympathetic hyperactivity post-myocardial infarction: Roles of METTL3-mediated m&lt;sup>6&lt;/sup> A methylation.</name><description>Ventricular arrhythmias (VAs) triggers by sympathetic nerve hyperactivity contribute to sudden cardiac death in myocardial infarction (MI) patients. Microglia-mediated inflammation in the paraventricular nucleus (PVN) is involved in sympathetic hyperactivity after MI. N6-methyladenosine (m&lt;sup>6&lt;/sup> A), the most prevalent mRNA and epigenetic modification, is critical for mediating cell inflammation. We aimed to explore whether METTL3-mediated m&lt;sup>6&lt;/sup> A modification is involved in microglia-mediated sympathetic hyperactivity after MI in the PVN. MI model was established by left coronary artery ligation. METTL3-mediated m&lt;sup>6&lt;/sup> A modification was markedly increased in the PVN at 3 days after MI, and METTL3 was primarily located in microglia by immunofluorescence. RNA-seq, MeRIP</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-04-04T20:23:56.575Z</modification><creation>2025-04-04T20:23:56.575Z</creation></dates><accession>S-EPMC8831944</accession><cross_references><pubmed>35040253</pubmed><doi>10.1111/jcmm.17183</doi></cross_references></HashMap>