{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["9"],"submitter":["Zhang H"],"pubmed_abstract":["The protective effects of mesenchymal stem cell (MSC)-based therapy for myocardial infarction (MI) are largely hampered as they age. Apelin is an endogenous ligand of its receptor APJ and plays an essential role in regulating multiple biological activities including MSC proliferation and survival. In this study, we investigated whether Apelin regulates MSC senescence and whether its overexpression could rejuvenate aged MSCs (AMSCs) to improve cardiac protection following infarction in mice. MSC senescence was evaluated by senescence-associated β-galactosidase assays. Apelin level was examined by western blotting. Autophagy was determined by transmission electron microscopy. The cardioprotective effect of AMSCs with Apelin overexpression (Apelin-AMSCs) was assessed in a mouse MI model. Apel"],"journal":["Frontiers in cell and developmental biology"],"pagination":["628463"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7960672"],"repository":["biostudies-literature"],"pubmed_title":["Apelin Rejuvenates Aged Human Mesenchymal Stem Cells by Regulating Autophagy and Improves Cardiac Protection After Infarction."],"pmcid":["PMC7960672"],"pubmed_authors":["Shi L","Zhao C","Liang X","Jiang G","Zhang H","Hu B","Li M","Li X","Zheng H","Ding Y","Hong Y","Zhang Y","Cui Z","Lin F","Wei L"],"additional_accession":[]},"is_claimable":false,"name":"Apelin Rejuvenates Aged Human Mesenchymal Stem Cells by Regulating Autophagy and Improves Cardiac Protection After Infarction.","description":"The protective effects of mesenchymal stem cell (MSC)-based therapy for myocardial infarction (MI) are largely hampered as they age. Apelin is an endogenous ligand of its receptor APJ and plays an essential role in regulating multiple biological activities including MSC proliferation and survival. In this study, we investigated whether Apelin regulates MSC senescence and whether its overexpression could rejuvenate aged MSCs (AMSCs) to improve cardiac protection following infarction in mice. MSC senescence was evaluated by senescence-associated β-galactosidase assays. Apelin level was examined by western blotting. Autophagy was determined by transmission electron microscopy. The cardioprotective effect of AMSCs with Apelin overexpression (Apelin-AMSCs) was assessed in a mouse MI model. Apel","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021","modification":"2025-04-22T10:49:50.406Z","creation":"2025-04-05T23:40:08.591Z"},"accession":"S-EPMC7960672","cross_references":{"pubmed":["33738284"],"doi":["10.3389/fcell.2021.628463"]}}