{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Qi L"],"funding":["China Postdoctoral Science Foundation","National Natural Science Foundation of China"],"pagination":["1264-1280"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8831944"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(4)"],"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<sup>6</sup> A), the most prevalent mRNA and epigenetic modification, is critical for mediating cell inflammation. We aimed to explore whether METTL3-mediated m<sup>6</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<sup>6</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"],"journal":["Journal of cellular and molecular medicine"],"pubmed_title":["New insights into the central sympathetic hyperactivity post-myocardial infarction: Roles of METTL3-mediated m<sup>6</sup> A methylation."],"pmcid":["PMC8831944"],"funding_grant_id":["2016M602154","81870253","882070345"],"pubmed_authors":["Qi L","Li P","Yan S","Wang K","Zhao Y","Shi Y","Li X","Li Y","Feng M","Hu H","Lyu H","Xue M","Wang Y","Yin J"],"additional_accession":[]},"is_claimable":false,"name":"New insights into the central sympathetic hyperactivity post-myocardial infarction: Roles of METTL3-mediated m<sup>6</sup> A methylation.","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<sup>6</sup> A), the most prevalent mRNA and epigenetic modification, is critical for mediating cell inflammation. We aimed to explore whether METTL3-mediated m<sup>6</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<sup>6</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","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-04-04T20:23:56.575Z","creation":"2025-04-04T20:23:56.575Z"},"accession":"S-EPMC8831944","cross_references":{"pubmed":["35040253"],"doi":["10.1111/jcmm.17183"]}}