ArticleProceedings of the National Academy of Sciences of the United States of America2021
A role for Sfrp2 in cardiomyogenesis in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Cell-cycle regulation of sarcomere integrity-Role for Actn2 phosphorylation.Physiological reports · 2026Article
- Secreted Frizzled-Related Protein 2 Promotes Osteogenic Differentiation and Bone Regeneration in Perthes Disease When Targeted by miR-106a-5p.Journal of cellular and molecular medicine · 2025Article
- FoxO3 controls cardiomyocyte proliferation and heart regeneration by regulating Sfrp2 expression in postnatal mice.Nature communications · 2025Article
- SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing.Frontiers in immunology · 2024Article
- Article
- Novel method of differentiating human induced pluripotent stem cells to mature cardiomyocytes via Sfrp2.Scientific reports · 2023Article
- Wnt Signaling in Heart Development and Regeneration.Current cardiology reports · 2022Review
- Biallelic DNAH9 mutations are identified in Chinese patients with defective left-right patterning and cilia-related complex congenital heart disease.Human genetics · 2022Article
- CircCEMIP promotes anoikis-resistance by enhancing protective autophagy in prostate cancer cells.Journal of experimental & clinical cancer research : CR · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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 Sfrp2 to promote cardiomyogenesis was further supported by tracking EdU-labeled cells. In addition, Sfrp2 did not promote the formation of new cardiomyocytes when the cKit(+) cell population was selectively ablated in vivo using a diphtheria toxin receptor-diphtheria toxin model. Notably, Sfrp2-induced cardiomyogenesis was associated with significant functional improvements in a cardiac injury model. In summary, our study further demonstrates the importance of Sfrp2 in cardiomyogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.