ArticleScientific reports2017
Fam64a is a novel cell cycle promoter of hypoxic fetal cardiomyocytes in mice.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Phosphorescence lifetime microscopy and contrast-enhanced ultrasound imaging revealed strong left-to-right intraventricular shunt in anesthetized Xenopus laevis.The journal of physiological sciences : JPS · 2026Article
- FAM64A Potentiates Bladder Carcinoma Tumorigenesis and Metastasis Through PI3K/mTORC2/AKT Pathway Activation.Cancers · 2026Article
- CCDC141 is a Connectin/Titin and Nesprin-1 binding protein that adapts cardiomyocytes to mechanical stress.Communications biology · 2025Article
- FAM64A silencing inhibits the proliferation, migration, invasion, and epithelial-mesenchymal transition in ovarian cancer cells via activating Hippo pathway.Discover oncology · 2025Article
- FAM64A regulates the malignant phenotype and tumor microenvironment of non-small cell lung cancer by activating the JAK/STAT3/PDL1 axis.Journal of molecular histology · 2025Article
- Transition from fetal to postnatal state in the heart: Crosstalk between metabolism and regeneration.Development, growth & differentiation · 2024Review
- Loss of connectin novex-3 leads to heart dysfunction associated with impaired cardiomyocyte proliferation and abnormal nuclear mechanics.Scientific reports · 2024Article
- Cardiac regeneration: Pre-existing cardiomyocyte as the hub of novel signaling pathway.Genes & diseases · 2024Review
- Clinical diagnostic value of PIMREG on liver cancer cell phenotype and tumorigenic ability in nude mice.American journal of translational research · 2024Article
- Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart-Part II: Molecular Mechanisms of Cardiac Regeneration.Journal of cardiovascular development and disease · 2023Review
- Cell Cycle-Related FAM64A Could be Activated by TGF-β Signaling to Promote Glioma Progression.Cellular and molecular neurobiology · 2023Article
- eSPRESSO: topological clustering of single-cell transcriptomics data to reveal informative genes for spatio-temporal architectures of cells.BMC bioinformatics · 2023Article
- Proliferation and Maturation: Janus and the Art of Cardiac Tissue Engineering.Circulation research · 2023Review
- Metabolic Determinants of Cardiomyocyte Proliferation.Stem cells (Dayton, Ohio) · 2022Article
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- Cardiac Remodeling and Repair: Recent Approaches, Advancements, and Future Perspective.International journal of molecular sciences · 2021Review
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- Pan-Cancer Analysis of PIMREG as a Biomarker for the Prognostic and Immunological Role.Frontiers in genetics · 2021Article
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Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fetal cardiomyocytes actively proliferate to form the primitive heart in utero in mammals, but they stop dividing shortly after birth. The identification of essential molecules maintaining this active cardiomyocyte proliferation is indispensable for potential adult heart regeneration. A recent study has shown that this proliferation depends on a low fetal oxygen condition before the onset of breathing at birth. We have established an isolation protocol for mouse fetal cardiomyocytes, performed under strict low oxygen conditions to mimic the intrauterine environment, that gives the highest proliferative activities thus far reported. Oxygen exposure during isolation/culture markedly inhibited cell division and repressed cell cycle-promoting genes, and subsequent genome-wide analysis identified Fam64a as a novel regulatory molecule. Fam64a was abundantly expressed in hypoxic fetal cardiomyocyte nuclei, but this expression was drastically repressed by oxygen exposure, and in postnatal cardiomyocytes following the onset of breathing and the resulting elevation of oxygen tension. Fam64a knockdown inhibited and its overexpression enhanced cardiomyocyte proliferation. Expression of a non-degradable Fam64a mutant suggested that optimum Fam64a expression and subsequent degradation by anaphase-promoting complex/cyclosome (APC/C) during the metaphase-to-anaphase transition are required for fetal cardiomyocyte division. We propose that Fam64a is a novel cell cycle promoter of hypoxic fetal cardiomyocytes in mice.
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