{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Slone S"],"funding":["American Heart Association","American Heart Association (AHA)","National Heart, Lung, and Blood Institute","NHLBI NIH HHS","HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)","National Cancer Institute","NCI NIH HHS","American Heart Association Career Development Grant","HHS | NIH | National Cancer Institute (NCI)","American Heart Association Postdoctoral Fellowship"],"pagination":["e70433"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11908633"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(6)"],"pubmed_abstract":["The RNA-binding protein human antigen R (HuR) has been shown to reduce cardiac remodeling following both myocardial infarction and cardiac pressure overload, but the full extent of the HuR-dependent mechanisms within cells of the myocardium has yet to be elucidated. Wild-type mice were subjected to 30 min of cardiac ischemia (via LAD occlusion) and treated with a novel small molecule inhibitor of HuR at the time of reperfusion, followed by direct in vivo assessment of cardiac structure and function. Direct assessment of HuR-dependent mechanisms was done in vitro using neonatal rat ventricular myocytes (NRVMs) and bone marrow-derived macrophages (BMDMs). HuR activity is increased within 2 h after ischemia/reperfusion (I/R) and is necessary for early post-I/R inflammatory gene expression in "],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["HuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response."],"pmcid":["PMC11908633"],"funding_grant_id":["R01 CA243445","HL148598","HL125204","R01 HL132111","1029875","23CDA1052132","CA243445","PRE35230020","CDA34110117","R33 CA252158","20POST35200267","CA191785","HL132111","R01 HL166326","PRE35210795","HL166326","R01 HL158671","CA252158","F31‐HL170636","F31-HL170636"],"pubmed_authors":["Slone S","Xu L","Green LC","Kanisicak O","Aube J","Anthony SR","Alam P","Acharya P","Kasprovic DA","Reynolds K","Li Z","Owens AP","Jaggers RM","Roy S","Parkins S","Nieman ML","Lorenz JN","Tranter M","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"HuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response.","description":"The RNA-binding protein human antigen R (HuR) has been shown to reduce cardiac remodeling following both myocardial infarction and cardiac pressure overload, but the full extent of the HuR-dependent mechanisms within cells of the myocardium has yet to be elucidated. Wild-type mice were subjected to 30 min of cardiac ischemia (via LAD occlusion) and treated with a novel small molecule inhibitor of HuR at the time of reperfusion, followed by direct in vivo assessment of cardiac structure and function. Direct assessment of HuR-dependent mechanisms was done in vitro using neonatal rat ventricular myocytes (NRVMs) and bone marrow-derived macrophages (BMDMs). HuR activity is increased within 2 h after ischemia/reperfusion (I/R) and is necessary for early post-I/R inflammatory gene expression in ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-02T11:59:14.512Z","creation":"2025-04-06T22:13:24.627Z"},"accession":"S-EPMC11908633","cross_references":{"pubmed":["40085190"],"doi":["10.1096/fj.202400532RRR"]}}