<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liao YH</submitter><funding>National Basic Research Program of China</funding><funding>NHLBI NIH HHS</funding><funding>National Natural Science Foundation of China</funding><funding>National Institutes of Health</funding><pagination>420-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3262985</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>59(4)</volume><pubmed_abstract>&lt;h4>Objectives&lt;/h4>This study tested whether interleukin (IL)-17A is involved in the pathogenesis of mouse myocardial ischemia/reperfusion (I/R) injury and investigated the mechanisms.&lt;h4>Background&lt;/h4>Inflammatory processes play a major role in myocardial I/R injury. We recently identified IL-17A as an important cytokine in inflammatory cardiovascular diseases such as atherosclerosis and viral myocarditis. However, its role in myocardial I/R injury remains unknown.&lt;h4>Methods&lt;/h4>The involvement of IL-17A was assessed in functional assays in mouse myocardial I/R injury by neutralization/repletion or genetic deficiency of IL-17A, and its mechanism on cardiomyocyte apoptosis and neutrophil infiltration were further studied in vivo and in vitro.&lt;h4>Results&lt;/h4>Interleukin-17A was elevated a</pubmed_abstract><journal>Journal of the American College of Cardiology</journal><pubmed_title>Interleukin-17A contributes to myocardial ischemia/reperfusion injury by regulating cardiomyocyte apoptosis and neutrophil infiltration.</pubmed_title><pmcid>PMC3262985</pmcid><funding_grant_id>R01 HL081090-04</funding_grant_id><funding_grant_id>R01 HL088547</funding_grant_id><funding_grant_id>HL88547</funding_grant_id><funding_grant_id>R01 HL060942</funding_grant_id><funding_grant_id>HL81090</funding_grant_id><funding_grant_id>30871067</funding_grant_id><funding_grant_id>R01 HL081090</funding_grant_id><funding_grant_id>HL60942</funding_grant_id><funding_grant_id>R01 HL088547-04</funding_grant_id><funding_grant_id>81170303</funding_grant_id><funding_grant_id>R01 HL060942-13</funding_grant_id><pubmed_authors>Jevallee H</pubmed_authors><pubmed_authors>Zhou SF</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Iwakura Y</pubmed_authors><pubmed_authors>Cheng X</pubmed_authors><pubmed_authors>Yuan J</pubmed_authors><pubmed_authors>Yan XX</pubmed_authors><pubmed_authors>Liao YH</pubmed_authors><pubmed_authors>Tang TT</pubmed_authors><pubmed_authors>Xia N</pubmed_authors><pubmed_authors>Xiao H</pubmed_authors><pubmed_authors>Wei F</pubmed_authors><pubmed_authors>Nie SF</pubmed_authors><pubmed_authors>Shi GP</pubmed_authors><pubmed_authors>Lv BJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interleukin-17A contributes to myocardial ischemia/reperfusion injury by regulating cardiomyocyte apoptosis and neutrophil infiltration.</name><description>&lt;h4>Objectives&lt;/h4>This study tested whether interleukin (IL)-17A is involved in the pathogenesis of mouse myocardial ischemia/reperfusion (I/R) injury and investigated the mechanisms.&lt;h4>Background&lt;/h4>Inflammatory processes play a major role in myocardial I/R injury. We recently identified IL-17A as an important cytokine in inflammatory cardiovascular diseases such as atherosclerosis and viral myocarditis. However, its role in myocardial I/R injury remains unknown.&lt;h4>Methods&lt;/h4>The involvement of IL-17A was assessed in functional assays in mouse myocardial I/R injury by neutralization/repletion or genetic deficiency of IL-17A, and its mechanism on cardiomyocyte apoptosis and neutrophil infiltration were further studied in vivo and in vitro.&lt;h4>Results&lt;/h4>Interleukin-17A was elevated a</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Jan</publication><modification>2025-04-05T13:10:39.878Z</modification><creation>2019-03-27T00:48:16Z</creation></dates><accession>S-EPMC3262985</accession><cross_references><pubmed>22261166</pubmed><doi>10.1016/j.jacc.2011.10.863</doi></cross_references></HashMap>