{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gao F"],"funding":["An- hui Natural Fund General Project"],"pagination":["33"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8908691"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["28(1)"],"pubmed_abstract":["<h4>Objective</h4>Long non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia-reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis.<h4>Methods</h4>miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury was measured. Mice with I/R injury were injected with the gene expression-modified vectors, after which cardiac function, hemodynamics, myocardial enzyme, oxidative stress, and cardiomyocyte apoptosis were analyzed.<h4>Results</h4>I/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice.<h4>Conclusion</h4>LINC00461 knockdown attenuates myocardial I/R injury via elevating miR-185-3p expression to suppress Myd88 expression."],"journal":["Molecular medicine (Cambridge, Mass.)"],"pubmed_title":["LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88."],"pmcid":["PMC8908691"],"funding_grant_id":["2008085MH239"],"pubmed_authors":["Li Y","Luo Z","Ma M","Hu G","Liang Y","Xu B","Lin X","Wang X","Gao F","Fan T"],"additional_accession":[]},"is_claimable":false,"name":"LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88.","description":"<h4>Objective</h4>Long non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia-reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis.<h4>Methods</h4>miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury was measured. Mice with I/R injury were injected with the gene expression-modified vectors, after which cardiac function, hemodynamics, myocardial enzyme, oxidative stress, and cardiomyocyte apoptosis were analyzed.<h4>Results</h4>I/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice.<h4>Conclusion</h4>LINC00461 knockdown attenuates myocardial I/R injury via elevating miR-185-3p expression to suppress Myd88 expression.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2025-04-04T20:50:28.988Z","creation":"2025-04-04T20:50:28.988Z"},"accession":"S-EPMC8908691","cross_references":{"pubmed":["35272621"],"doi":["10.1186/s10020-022-00452-1"]}}