ArticleNature cardiovascular research2022
Cre toxicity in mouse models of cardiovascular physiology and disease.
Article in Nature cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed.
- Loss of the Coronary Artery Disease Risk GeneCirculation · 2026Article
- Ckmm-Cre transgenic mice maintain phenotypic and cardiac mitochondrial homeostasis during ketogenic feeding.Molecular and cellular biochemistry · 2026Article
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- MCC links Wnt/PCP signaling to endothelial polarity and vascular remodeling.Angiogenesis · 2026Article
- Contemporary Endothelial Genome Editing Technologies: Towards Precision Genetic Medicine for Vascular Diseases.International journal of molecular sciences · 2026Review
- CreER activation transiently disrupts angiogenesis by reducing proliferation and promoting apoptosis in vascular endothelial cells.Angiogenesis · 2026Article
- Article
- Apolipoprotein D, a Novel Ligand for CD36, Is Essential for Blood-Brain Barrier Integrity.Circulation · 2026Article
- Restoration of RBM22 overcomes the transcriptional and epigenetic barriers of cardiomyocyte proliferation for heart regeneration.Nature communications · 2026Article
- Cooperative ETS transcription factors are required for lymphatic endothelial cell integrity and resilience.The Journal of clinical investigation · 2026Article
- Article
- Some Basics on Innate Neuroimmunology for Nonspecialists.Neuroimmunomodulation · 2026Review
- Targeting SRPK3 Attenuates Cardiac Hypertrophy and Heart Failure by Improving Mitochondrial Bioenergetics through mRNA Splicing and Decay.Research (Washington, D.C.) · 2026Article
- A guide to cell-type-specific Cre mouse models in atherosclerosis: from background strains to future directions.Frontiers in cardiovascular medicine · 2026Review
- Spatial Chromatin Organization Across the Cell Cycle: Insights from Auxin-Inducible Protein Depletion.Cells · 2025Review
- Myeloid GPSM1 regulates atherosclerosis progression by governing monocyte and macrophage activation and chemotaxis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Emergence of endothelial subtypes and role of cell cycle control in arterial-venous specification during embryonic vascular development.Cell reports · 2025Article
- DNA double-stranded breaks, a hallmark of aging, defined at the nucleotide resolution, are increased and associated with transcription in the cardiac myocytes in LMNA-cardiomyopathy.Cardiovascular research · 2025Article
- Restoring AIBP expression in the retina provides neuroprotection in glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Genetic Animal Models of Cardiovascular Pathologies.Biomedicines · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The Cre-LoxP system provides a widely used method for studying gene requirements in the mouse as the main mammalian genetic model organism. To define the molecular and cellular mechanisms that underlie cardiovascular development, function and disease, various mouse strains have been engineered that allow Cre-LoxP-mediated gene targeting within specific cell types of the cardiovascular system. Despite the usefulness of this system, evidence is accumulating that Cre activity can have toxic effects in cells, independently of its ability to recombine pairs of engineered LoxP sites in target genes. Here, we have gathered published evidence for Cre toxicity in cells and tissues relevant to cardiovascular biology and provide an overview of mechanisms proposed to underlie Cre toxicity. Based on this knowledge, we propose that each study utilising the Cre-LoxP system to investigate gene function in the cardiovascular system should incorporate appropriate controls to account for Cre toxicity.
Identifiers
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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.