ArticleFrontiers in cardiovascular medicine2022
HRas and Myc synergistically induce cell cycle progression and apoptosis of murine cardiomyocytes.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Bench to Bedside: Insights from Large Animal Models and Emerging Clinical Trials of Endogenous Cardiac Regeneration and Repair.Journal of cardiovascular translational research · 2026Review
- Revitalizing the heart: strategies and tools for cardiomyocyte regeneration post-myocardial infarction.NPJ Regenerative medicine · 2025Review
- HRAS Induces Ferroptosis through Upregulating HSPB1 in Hepatocellular Carcinoma.Combinatorial chemistry & high throughput screening · 2025Article
- Manipulating Myc for reparative regeneration.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Aim: Adult mammalian cardiomyocytes are incapable of significant proliferation, limiting regeneration after myocardial injury. Overexpression of the transcription factor Myc has been shown to drive proliferation in the adult mouse heart, but only when combined with Cyclin T1. As constitutive HRas activity has been shown to stabilise Cyclin T1 Methods and results: Using a genetically modified mouse model, we confirmed that constitutive HRas activity (HRas Conclusion: Co-expression of Cyclin T1 and Myc may be a therapeutically tractable approach for cardiomyocyte neo-genesis post injury, while cell death induced by HRas
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Registered trials
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