<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gomez JA</submitter><funding>HHS | NIH | National Heart, Lung, and Blood Institute</funding><pagination>e2103676118</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8379963</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>118(33)</volume><pubmed_abstract>Cardiomyogenesis, the process by which the body generates cardiomyocytes, is poorly understood. We have recently shown that Sfrp2 promotes cardiomyogenesis in vitro. The objective of this study was to determine if Sfrp2 would similarly promote cardiomyogenesis in vivo. To test this hypothesis, we tracked multipotent cKit(+) cells in response to Sfrp2 treatment. In control adult mice, multipotent cKit(+) cells typically differentiated into endothelial cells but not cardiomyocytes. In contrast, Sfrp2 switched the fate of these cells. Following Sfrp2 injection, multipotent cKit(+) cells differentiated solely into cardiomyocytes. Sfrp2-derived cardiomyocytes integrated into the myocardium and exhibited identical physiological properties to preexisting native cardiomyocytes. The ability of Sfrp</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>A role for Sfrp2 in cardiomyogenesis in vivo.</pubmed_title><pmcid>PMC8379963</pmcid><funding_grant_id>RO1 HL35610</funding_grant_id><pubmed_authors>Gomez JA</pubmed_authors><pubmed_authors>Hodgkinson CP</pubmed_authors><pubmed_authors>Payne A</pubmed_authors><pubmed_authors>Pratt RE</pubmed_authors><pubmed_authors>Dzau VJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>A role for Sfrp2 in cardiomyogenesis in vivo.</name><description>Cardiomyogenesis, the process by which the body generates cardiomyocytes, is poorly understood. We have recently shown that Sfrp2 promotes cardiomyogenesis in vitro. The objective of this study was to determine if Sfrp2 would similarly promote cardiomyogenesis in vivo. To test this hypothesis, we tracked multipotent cKit(+) cells in response to Sfrp2 treatment. In control adult mice, multipotent cKit(+) cells typically differentiated into endothelial cells but not cardiomyocytes. In contrast, Sfrp2 switched the fate of these cells. Following Sfrp2 injection, multipotent cKit(+) cells differentiated solely into cardiomyocytes. Sfrp2-derived cardiomyocytes integrated into the myocardium and exhibited identical physiological properties to preexisting native cardiomyocytes. The ability of Sfrp</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2025-04-05T14:05:42.124Z</modification><creation>2025-04-05T14:05:42.124Z</creation></dates><accession>S-EPMC8379963</accession><cross_references><pubmed>34380738</pubmed><doi>10.1073/pnas.2103676118</doi></cross_references></HashMap>