<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Luo Y</submitter><funding>National Key R&amp;amp;D Program of China</funding><funding>NCATS NIH HHS</funding><funding>National Natural Science Foundation of China</funding><funding>National Institutes of Health</funding><funding>NIH</funding><funding>NIGMS NIH HHS</funding><pagination>1881-1897</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7070165</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>177(8)</volume><pubmed_abstract>&lt;h4>Background and purpose&lt;/h4>Lipopolysaccharides (LPS), an outer membrane component of Gram-negative bacteria, triggers myocardial anomalies in sepsis. Recent findings indicated a role for inflammatory cytokine MIF and its receptor, CD74, in septic organ injury, although little is known of the role of MIF-CD74 in septic cardiomyopathy.&lt;h4>Experimental approach&lt;/h4>This study evaluated the impact of CD74 ablation on endotoxaemia-induced cardiac anomalies. Echocardiographic, cardiomyocyte contractile and intracellular Ca&lt;sup>2+&lt;/sup> properties were examined.&lt;h4>Key results&lt;/h4>Our data revealed compromised cardiac function (lower fractional shortening, enlarged LV end systolic diameter, decreased peak shortening, maximal velocity of shortening/relengthening, prolonged duration of relength</pubmed_abstract><journal>British journal of pharmacology</journal><pubmed_title>CD74 knockout protects against LPS-induced myocardial contractile dysfunction through AMPK-Skp2-SUV39H1-mediated demethylation of BCLB.</pubmed_title><pmcid>PMC7070165</pmcid><funding_grant_id>81570225</funding_grant_id><funding_grant_id>81372055</funding_grant_id><funding_grant_id>81522004</funding_grant_id><funding_grant_id>T32 GM007205</funding_grant_id><funding_grant_id>UL1 TR001863</funding_grant_id><funding_grant_id>81571895</funding_grant_id><funding_grant_id>81770261</funding_grant_id><funding_grant_id>2017YFA0506000</funding_grant_id><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Ren J</pubmed_authors><pubmed_authors>Yang M</pubmed_authors><pubmed_authors>Bucala R</pubmed_authors><pubmed_authors>Dong M</pubmed_authors><pubmed_authors>Pei Z</pubmed_authors><pubmed_authors>Luo Y</pubmed_authors><pubmed_authors>Fan C</pubmed_authors></additional><is_claimable>false</is_claimable><name>CD74 knockout protects against LPS-induced myocardial contractile dysfunction through AMPK-Skp2-SUV39H1-mediated demethylation of BCLB.</name><description>&lt;h4>Background and purpose&lt;/h4>Lipopolysaccharides (LPS), an outer membrane component of Gram-negative bacteria, triggers myocardial anomalies in sepsis. Recent findings indicated a role for inflammatory cytokine MIF and its receptor, CD74, in septic organ injury, although little is known of the role of MIF-CD74 in septic cardiomyopathy.&lt;h4>Experimental approach&lt;/h4>This study evaluated the impact of CD74 ablation on endotoxaemia-induced cardiac anomalies. Echocardiographic, cardiomyocyte contractile and intracellular Ca&lt;sup>2+&lt;/sup> properties were examined.&lt;h4>Key results&lt;/h4>Our data revealed compromised cardiac function (lower fractional shortening, enlarged LV end systolic diameter, decreased peak shortening, maximal velocity of shortening/relengthening, prolonged duration of relength</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Apr</publication><modification>2026-05-03T20:02:55.118Z</modification><creation>2022-02-10T17:11:27.842Z</creation></dates><accession>S-EPMC7070165</accession><cross_references><pubmed>31877229</pubmed><doi>10.1111/bph.14959</doi></cross_references></HashMap>