{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jeyabal P"],"funding":["American Heart Association","NHLBI NIH HHS","National Institutes of Health"],"pagination":["423-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4818978"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["471(4)"],"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"],"journal":["Biochemical and biophysical research communications"],"pubmed_title":["MicroRNA-9 inhibits hyperglycemia-induced pyroptosis in human ventricular cardiomyocytes by targeting ELAVL1."],"pmcid":["PMC4818978"],"funding_grant_id":["HL091983","P01 HL108795","R01 HL126186","R01 HL095874","R01 HL105597","HL108806","R01 HL116729","15POST25710392","R01 HL091983","R01 HL053354","HL053354","HL108795","P01 HL108806","R37 HL053354","1R01HL116729","25860041"],"pubmed_authors":["Thandavarayan RA","Jeyabal P","Krishnamurthy P","Joladarashi D","Krishnamurthy S","Suresh Babu S","Bhimaraj A","Youker KA","Kishore R"],"additional_accession":[]},"is_claimable":false,"name":"MicroRNA-9 inhibits hyperglycemia-induced pyroptosis in human ventricular cardiomyocytes by targeting ELAVL1.","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","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Mar","modification":"2025-04-04T00:12:37.113Z","creation":"2019-03-27T03:11:04Z"},"accession":"S-EPMC4818978","cross_references":{"pubmed":["26898797"],"doi":["10.1016/j.bbrc.2016.02.065"]}}