<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jeyabal P</submitter><funding>American Heart Association</funding><funding>NHLBI NIH HHS</funding><funding>National Institutes of Health</funding><pagination>423-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4818978</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>471(4)</volume><pubmed_abstract>Diabetic cardiomyopathy is a common complication in patients with diabetes and is associated with underlying chronic inflammation and cardiac cell death, subsequently leading to heart failure (HF). ELAV-like protein 1 (ELAVL1) plays a critical role in the progression of inflammation and HF. However the role of ELAVL-1 in inflammation induced cardiac cell death (pyroptosis) under hyperglycemic condition remains elusive. Our data demonstrates that ELAVL1 expression augmented with a concomitant increase in caspase-1 and IL-1 beta expression in human hearts and human ventricular cardiomyocytes under hyperglycemic condition. Furthermore, ELAVL1 knockdown abrogates TNF-α induced canonical pyroptosis via NLRP3, caspase-1 and IL-1beta suppression. Bioinformatics analysis and target validation assa</pubmed_abstract><journal>Biochemical and biophysical research communications</journal><pubmed_title>MicroRNA-9 inhibits hyperglycemia-induced pyroptosis in human ventricular cardiomyocytes by targeting ELAVL1.</pubmed_title><pmcid>PMC4818978</pmcid><funding_grant_id>HL091983</funding_grant_id><funding_grant_id>P01 HL108795</funding_grant_id><funding_grant_id>R01 HL126186</funding_grant_id><funding_grant_id>R01 HL095874</funding_grant_id><funding_grant_id>R01 HL105597</funding_grant_id><funding_grant_id>HL108806</funding_grant_id><funding_grant_id>R01 HL116729</funding_grant_id><funding_grant_id>15POST25710392</funding_grant_id><funding_grant_id>R01 HL091983</funding_grant_id><funding_grant_id>R01 HL053354</funding_grant_id><funding_grant_id>HL053354</funding_grant_id><funding_grant_id>HL108795</funding_grant_id><funding_grant_id>P01 HL108806</funding_grant_id><funding_grant_id>R37 HL053354</funding_grant_id><funding_grant_id>1R01HL116729</funding_grant_id><funding_grant_id>25860041</funding_grant_id><pubmed_authors>Thandavarayan RA</pubmed_authors><pubmed_authors>Jeyabal P</pubmed_authors><pubmed_authors>Krishnamurthy P</pubmed_authors><pubmed_authors>Joladarashi D</pubmed_authors><pubmed_authors>Krishnamurthy S</pubmed_authors><pubmed_authors>Suresh Babu S</pubmed_authors><pubmed_authors>Bhimaraj A</pubmed_authors><pubmed_authors>Youker KA</pubmed_authors><pubmed_authors>Kishore R</pubmed_authors></additional><is_claimable>false</is_claimable><name>MicroRNA-9 inhibits hyperglycemia-induced pyroptosis in human ventricular cardiomyocytes by targeting ELAVL1.</name><description>Diabetic cardiomyopathy is a common complication in patients with diabetes and is associated with underlying chronic inflammation and cardiac cell death, subsequently leading to heart failure (HF). ELAV-like protein 1 (ELAVL1) plays a critical role in the progression of inflammation and HF. However the role of ELAVL-1 in inflammation induced cardiac cell death (pyroptosis) under hyperglycemic condition remains elusive. Our data demonstrates that ELAVL1 expression augmented with a concomitant increase in caspase-1 and IL-1 beta expression in human hearts and human ventricular cardiomyocytes under hyperglycemic condition. Furthermore, ELAVL1 knockdown abrogates TNF-α induced canonical pyroptosis via NLRP3, caspase-1 and IL-1beta suppression. Bioinformatics analysis and target validation assa</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Mar</publication><modification>2025-04-04T00:12:37.113Z</modification><creation>2019-03-27T03:11:04Z</creation></dates><accession>S-EPMC4818978</accession><cross_references><pubmed>26898797</pubmed><doi>10.1016/j.bbrc.2016.02.065</doi></cross_references></HashMap>