{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Paik DT"],"funding":["NEI NIH HHS","NICHD NIH HHS","NIDDK NIH HHS","NHLBI NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["804-16"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4600464"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["117(9)"],"pubmed_abstract":["<h4>Rationale</h4>Myocardial infarction causes irreversible tissue damage, leading to heart failure. We recently discovered that canonical Wnt signaling and the Wnt10b ligand are strongly induced in mouse hearts after infarction. Wnt10b regulates cell fate in various organs, but its role in the heart is unknown.<h4>Objective</h4>To investigate the effect of Wnt10b gain-of-function on cardiac repair mechanisms and to assess its potential to improve ventricular function after injury.<h4>Methods and results</h4>Histological and molecular analyses showed that Wnt10b is expressed in cardiomyocytes and localized in the intercalated discs of mouse and human hearts. After coronary artery ligation or cryoinjury in mice, Wnt10b is strongly and transiently induced in peri-infarct cardiomyocytes durin"],"journal":["Circulation research"],"pubmed_title":["Wnt10b Gain-of-Function Improves Cardiac Repair by Arteriole Formation and Attenuation of Fibrosis."],"pmcid":["PMC4600464"],"funding_grant_id":["HL100398","R01 HL095787","T32GM07347","DK58404","U24 DK059637","DK59637","P30 DK058404","P60 DK020593","T32HL007411","T32 GM007347","R01 HL083958","P30 EY008126","CA68485","U01 HL100398","DK20593","HL083958","EY08126","P30 DK020593","P30 CA068485","HD15052","T32 HL007411","HL095787","P30 HD015052"],"pubmed_authors":["Ryzhov S","Sanders LN","Hatzopoulos AK","Rai M","Funke MJ","Aisagbonhi O","Feoktistov I","Paik DT"],"additional_accession":[]},"is_claimable":false,"name":"Wnt10b Gain-of-Function Improves Cardiac Repair by Arteriole Formation and Attenuation of Fibrosis.","description":"<h4>Rationale</h4>Myocardial infarction causes irreversible tissue damage, leading to heart failure. We recently discovered that canonical Wnt signaling and the Wnt10b ligand are strongly induced in mouse hearts after infarction. Wnt10b regulates cell fate in various organs, but its role in the heart is unknown.<h4>Objective</h4>To investigate the effect of Wnt10b gain-of-function on cardiac repair mechanisms and to assess its potential to improve ventricular function after injury.<h4>Methods and results</h4>Histological and molecular analyses showed that Wnt10b is expressed in cardiomyocytes and localized in the intercalated discs of mouse and human hearts. After coronary artery ligation or cryoinjury in mice, Wnt10b is strongly and transiently induced in peri-infarct cardiomyocytes durin","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Oct","modification":"2025-06-01T12:02:17.936Z","creation":"2019-03-27T01:59:50Z"},"accession":"S-EPMC4600464","cross_references":{"pubmed":["26338900"],"doi":["10.1161/circresaha.115.306886","10.1161/CIRCRESAHA.115.306886"]}}