biostudies-literatureSlone SAmerican Heart AssociationAmerican Heart Association (AHA)National Heart, Lung, and Blood InstituteNHLBI NIH HHSHHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)National Cancer InstituteNCI NIH HHSAmerican Heart Association Career Development GrantHHS | NIH | National Cancer Institute (NCI)American Heart Association Postdoctoral Fellowshipe70433https://www.ebi.ac.uk/biostudies/studies/S-EPMC11908633biostudies-literatureUnknown39(6)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 FASEB journal : official publication of the Federation of American Societies for Experimental BiologyHuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response.PMC11908633R01 CA243445HL148598HL125204R01 HL132111102987523CDA1052132CA243445PRE35230020CDA34110117R33 CA25215820POST35200267CA191785HL132111R01 HL166326PRE35210795HL166326R01 HL158671CA252158F31‐HL170636F31-HL170636Slone SXu LGreen LCKanisicak OAube JAnthony SRAlam PAcharya PKasprovic DAReynolds KLi ZOwens APJaggers RMRoy SParkins SNieman MLLorenz JNTranter MWu XfalseHuR inhibition reduces post-ischemic cardiac remodeling by dampening myocyte-dependent inflammatory gene expression and the innate immune response.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 2025-01-01T00:00:00Z2025 Mar2026-06-02T11:59:14.512Z2025-04-06T22:13:24.627ZS-EPMC119086334008519010.1096/fj.202400532RRR