ArticleMolecules (Basel, Switzerland)2019
Cardiac-Specific Cre Induces Age-Dependent Dilated Cardiomyopathy (DCM) in Mice.
Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Ckmm-Cre transgenic mice maintain phenotypic and cardiac mitochondrial homeostasis during ketogenic feeding.Molecular and cellular biochemistry · 2026Article
- Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.The Journal of clinical investigation · 2026Article
- Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2026Article
- MYH6-Cre Insertion Accelerates Cardiac Phenotype in Dystrophic D2-mdx Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Cardiac dysfunction related to cardiac mRNA and protein traffic impairment due to reduced unconventional motor protein myosin-5b expression.European heart journal · 2025Article
- Mechanisms underlying dilated cardiomyopathy associated with FKBP12 deficiency.The Journal of general physiology · 2025Article
- Cre recombinase affects calcium dynamics already in young mice.Frontiers in pharmacology · 2025Article
- SLMAP3 is essential for neurulation through mechanisms involving cytoskeletal elements, ABP, and PCP.Life science alliance · 2024Article
- Ubiquitin Ligase RBX2/SAG Regulates Mitochondrial Ubiquitination and Mitophagy.Circulation research · 2024Article
- Integrated analysis reveals the dysfunction of intercellular communication and metabolic signals in dilated cardiomyopathy.Heliyon · 2024Article
- MicroRNA205: A Key Regulator of Cardiomyocyte Transition from Proliferative to Hypertrophic Growth in the Neonatal Heart.International journal of molecular sciences · 2024Article
- Warning regarding hematological toxicity of tamoxifen activated CreERT2 in young Rosa26CreERT2 mice.Scientific reports · 2023Article
- Cardiac-Specific Expression of Cre Recombinase Leads to Age-Related Cardiac Dysfunction Associated with Tumor-like Growth of Atrial Cardiomyocyte and Ventricular Fibrosis and Ferroptosis.International journal of molecular sciences · 2023Article
- Animal models and animal-free innovations for cardiovascular research: current status and routes to be explored. Consensus document of the ESC Working Group on Myocardial Function and the ESC Working Group on Cellular Biology of the Heart.Cardiovascular research · 2022Article
- Cre toxicity in mouse models of cardiovascular physiology and disease.Nature cardiovascular research · 2022Article
- circHIPK3 prevents cardiac senescence by acting as a scaffold to recruit ubiquitin ligase to degrade HuR.Theranostics · 2022Article
- Metabolic remodeling precedes mTORC1-mediated cardiac hypertrophy.Journal of molecular and cellular cardiology · 2021Article
- Atg5 knockdown induces age-dependent cardiomyopathy which can be rescued by repeated remote ischemic conditioning.Basic research in cardiology · 2021Article
- Article
- Disordered autonomic function during exposure to moderate heat or exercise in a mouse model of Dravet syndrome.Neurobiology of disease · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The genetic modification of the mouse genome using the cre-lox system has been an invaluable tool in deciphering gene and protein function in a temporal and/or spatial manner. However, it has its pitfalls, as researchers have shown that the unregulated expression of cre recombinase can cause DNA damage, the consequences of which can be very detrimental to mouse health. Previously published literature on the most utilized cardiac-specific cre, αMHC-cre, mouse model exhibited a nonlethal hypertrophic cardiomyopathy (HCM) with aging. However, using the same αMHC-cre mice, we observed a cardiac pathology, resulting in complete lethality by 11 months of age. Echocardiography and histology revealed that the αMHC-cre mice were displaying symptoms of dilated cardiomyopathy (DCM) by seven months of age, which ultimately led to their demise in the absence of any HCM at any age. Molecular analysis showed that this phenotype was associated with the DNA damage response through the downregulation of activated p38 and increased expression of JNK, p53, and Bax, known inducers of myocyte death resulting in fibrosis. Our data urges strong caution when interpreting the phenotypic impact of gene responses using αMHC-cre mice, since a lethal DCM was induced by the cre driver in an age-dependent manner in this commonly utilized model system.
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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.