ArticleBasic research in cardiology2021
4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice.
Article in Basic research in cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Prolonged tamoxifen-enriched diet is associated with cardiomyopathy and nutritional frailty in mice.Experimental physiology · 2024Article
- TBC1D15 deficiency protects against doxorubicin cardiotoxicityActa pharmaceutica Sinica. B · 2023Article
- Fibroblast growth factor 18 alleviates stress-induced pathological cardiac hypertrophy in male mice.Nature communications · 2023Article
- PANoptosis is a prominent feature of desmoplakin cardiomyopathy.The journal of cardiovascular aging · 2023Article
- Optimization of tamoxifen-induced gene regulation in cardiovascular research.The journal of cardiovascular aging · 2022Article
- Effects of tamoxifen inducible MerCreMer on gene expression in cardiac myocytes in mice.The journal of cardiovascular aging · 2022Article
- The Pitfalls ofFrontiers in physiology · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Conditional, cell-type-specific transgenic mouse lines are of high value in cardiovascular research. A standard tool for cardiomyocyte-restricted DNA editing is the αMHC-MerCreMer/loxP system. However, there is an ongoing debate on the occurrence of cardiac side effects caused by unspecific Cre activity or related to tamoxifen/oil overload. Here, we investigated potential adverse effects of DNA editing by the αMHC-MerCreMer/loxP system in combination with a low-dose treatment protocol with the tamoxifen metabolite 4-hydroxytamoxifen (OH-Txf). αMHC-MerCreMer mice received intraperitoneally OH-Txf (20 mg/kg) for 5 or 10 days. These treatment protocols were highly efficient to induce DNA editing in adult mouse hearts. Multi-parametric magnetic resonance imaging revealed neither transient nor permanent effects on cardiac function during or up to 19 days after 5 day OH-Txf treatment. Furthermore, OH-Txf did not affect cardiac phosphocreatine/ATP ratios assessed by in vivo
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