ArticleCurrent research in physiology2019
Cardiac hypertrophy or failure? - A systematic evaluation of the transverse aortic constriction model in C57BL/6NTac and C57BL/6J substrains.
Article in Current research in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Novel Quality Metrics for Assessing the Reproducibility and Translational Relevance of Mouse Transverse Aortic Constriction Experiments: A Systematic Review.Journal of the American Heart Association · 2026Pooled it
- Optimized murine HFpEF models for translational preclinical studies.ESC heart failure · 2026Article
- Empagliflozin Attenuates Cardiac Fibrosis by Suppressing Fibroblast-Mediated C-C Motif Chemokine Ligand 2 Expression.Journal of the American Heart Association · 2026Article
- Editorial: Understanding the physiology of ageing.Current research in physiology · 2026Article
- Substrain-Dependent Differences in Doxorubicin-Induced Cardiotoxicity in Adult C57BL/6 Mice.Cardiovascular toxicology · 2025Article
- Electrical Remodeling of Pressure Overloaded Rat Heart Is Attenuated if Imposed During Proliferative Cardiac Growth.Acta physiologica (Oxford, England) · 2025Article
- MYH11 rare variant augments aortic growth and induces cardiac hypertrophy and heart failure with pressure overload.PLoS genetics · 2025Article
- Effect of Mouse (Mus musculus) Sex and C57BL/6 Substrain on Sensitivity to Isoflurane and Ketamine-Xylazine-Acepromazine Anesthesia.Journal of the American Association for Laboratory Animal Science : JAALAS · 2025Article
- Gain and loss of the centrosomal protein taxilin-beta influences cardiac proteostasis and stress.Journal of molecular and cellular cardiology · 2025Article
- Cardiometabolic Phenotype in HFpEF: Insights from Murine Models.Biomedicines · 2025Review
- Valerenic acid attenuates pathological myocardial hypertrophy by promoting the utilization of multiple substrates in the mitochondrial energy metabolism.Journal of advanced research · 2025Article
- The Role of Programmed Types of Cell Death in Pathogenesis of Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- Proteomics couples electrical remodelling to inflammation in a murine model of heart failure with sinus node dysfunction.Cardiovascular research · 2024Article
- Treatment with αvβ3-integrin-specific 29P attenuates pressure-overload induced cardiac remodelling after transverse aortic constriction in mice.Journal of molecular and cellular cardiology plus · 2024Article
- α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor.EMBO reports · 2024Article
- Modulation of miR-29 influences myocardial compliance likely through coordinated regulation of calcium handling and extracellular matrix.Molecular therapy. Nucleic acids · 2023Article
- Age-Related Shift in Cardiac and Metabolic Phenotyping Linked to Inflammatory Cytokines and Antioxidant Status in Mice.International journal of molecular sciences · 2023Article
- New drug discovery of cardiac anti-arrhythmic drugs: insights in animal models.Scientific reports · 2023Article
- Striated muscle-specific base editing enables correction of mutations causing dilated cardiomyopathy.Nature communications · 2023Article
- PKN2 deficiency leads both to prenatal 'congenital' cardiomyopathy and defective angiotensin II stress responses.The Biochemical journal · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe mouse model of transverse aortic constriction (TAC) has been widely used as a cardiac stress in the investigation of the molecular mechanisms of cardiac hypertrophy. Recently, the International Knockout Mouse Consortium has selected the C57BL/6NTac (BL/6N) mouse strain to generate null alleles for all mouse genes; however, a range of genetic and cardiac phenotypic differences have been reported between this substrain and the commonly used C57BL/6J (BL/6J) substrain. It has been reported by Garcia-Menendez and colleagues that 12-week C57BL/6NTac mice are susceptible to heart failure but little is known about the cardiac remodeling in this substrain as cardiac function progresses from compensation to decompensation.
methodsBL/6J and BL/6N mice were subjected to pressure overload via TAC. The impact of both age and duration of cardiac pressure overload induced by TAC on cardiac remodelling were systematically assessed.
resultsOur data showed that BL/6N mice developed eccentric hypertrophy with age- and time-dependent deterioration in cardiac function, accompanied by considerable interstitial fibrosis. In contrast, BL/6J mice were more resilient to TAC-induced cardiac stress and developed variable cardiac phenotypes independent of age and the duration of pressure overload. This was likely due to the greater variability in pre-TAC aortic arch dimension as measured by echocardiography. In addition to increased expression of brain natriuretic peptide and collagen gene type 1 and 3, BL/6N mice also had greater angiotensin II type 2 receptor (AT2R) gene expression than BL/6J counterparts at baseline and after 2-weeks TAC, which may contribute to the exacerbated interstitial fibrosis.
conclusionsBL/6N and BL/6J mice have very different responses to TAC stimulation and these differences should be taken into consideration when using the substrains to investigate the mechanisms of hypertrophy and heart failure.
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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.