{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yan W"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS","NIH HHS"],"pagination":["2162-2177"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5705403"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["136(22)"],"pubmed_abstract":["<h4>Background</h4>Cell therapy remains the most promising approach against ischemic heart injury. However, the poor survival of engrafted stem cells in the ischemic environment limits their therapeutic efficacy for cardiac repair after myocardial infarction. CTRP9 (C1q/tumor necrosis factor-related protein-9) is a novel prosurvival cardiokine with significantly downregulated expression after myocardial infarction. Here we tested a hypothesis that CTRP9 might be a cardiokine required for a healthy microenvironment promoting implanted stem cell survival and cardioprotection.<h4>Methods</h4>Mice were subjected to myocardial infarction and treated with adipose-derived mesenchymal stem cells (ADSCs, intramyocardial transplantation), CTRP9, or their combination. Survival, cardiac remodeling and"],"journal":["Circulation"],"pubmed_title":["C1q/Tumor Necrosis Factor-Related Protein-9 Regulates the Fate of Implanted Mesenchymal Stem Cells and Mobilizes Their Protective Effects Against Ischemic Heart Injury via Multiple Novel Signaling Pathways."],"pmcid":["PMC5705403"],"funding_grant_id":["R01 HL096686","R56 HL123404","S10 OD010408","R01 DK084171","R01 HL123404"],"pubmed_authors":["Tao L","Yan Z","Guo Y","Gan L","Lau WB","Ma XL","Wong GW","Guo R","Gao E","Koch WL","Wang Y","Yan W"],"additional_accession":[]},"is_claimable":false,"name":"C1q/Tumor Necrosis Factor-Related Protein-9 Regulates the Fate of Implanted Mesenchymal Stem Cells and Mobilizes Their Protective Effects Against Ischemic Heart Injury via Multiple Novel Signaling Pathways.","description":"<h4>Background</h4>Cell therapy remains the most promising approach against ischemic heart injury. However, the poor survival of engrafted stem cells in the ischemic environment limits their therapeutic efficacy for cardiac repair after myocardial infarction. CTRP9 (C1q/tumor necrosis factor-related protein-9) is a novel prosurvival cardiokine with significantly downregulated expression after myocardial infarction. Here we tested a hypothesis that CTRP9 might be a cardiokine required for a healthy microenvironment promoting implanted stem cell survival and cardioprotection.<h4>Methods</h4>Mice were subjected to myocardial infarction and treated with adipose-derived mesenchymal stem cells (ADSCs, intramyocardial transplantation), CTRP9, or their combination. Survival, cardiac remodeling and","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Nov","modification":"2025-04-26T06:55:30.732Z","creation":"2019-03-27T00:08:52Z"},"accession":"S-EPMC5705403","cross_references":{"pubmed":["28978553"],"doi":["10.1161/CIRCULATIONAHA.117.029557","10.1161/circulationaha.117.029557"]}}