ArticlePloS one2013
Mouse strain determines cardiac growth potential.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
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- Sex based cardiovascular differences in adult and middle-aged hypertensive schlager mice.Scientific reports · 2025Article
- Comparative phenotyping of C57BL/6J substrains reveals distinctive patterns of cardiac aging.GeroScience · 2025Article
- Metabolic Syndrome Nonalcoholic Steatohepatitis Male Mouse With Adeno-Associated Viral Renin as a Novel Model for Heart Failure With Preserved Ejection Fraction.Journal of the American Heart Association · 2024Article
- Revisiting Cardiac Biology in the Era of Single Cell and Spatial Omics.Circulation research · 2024Review
- Age-Related Shift in Cardiac and Metabolic Phenotyping Linked to Inflammatory Cytokines and Antioxidant Status in Mice.International journal of molecular sciences · 2023Article
- Genome-wide transcript and protein analysis highlights the role of protein homeostasis in the aging mouse heart.Genome research · 2022Article
- Naked mole-rats maintain cardiac function and body composition well into their fourth decade of life.GeroScience · 2022Article
- Altered Glycosylation in the Aging Heart.Frontiers in molecular biosciences · 2021Article
- Cross-Sectional Transcriptional Analysis of the Aging Murine Heart.Frontiers in molecular biosciences · 2020Article
- A personalized, multiomics approach identifies genes involved in cardiac hypertrophy and heart failure.NPJ systems biology and applications · 2018Article
- MicroRNA miR-301a is a novel cardiac regulator of Cofilin-2.PloS one · 2017Article
- RNAseq analysis of heart tissue from mice treated with atenolol and isoproterenol reveals a reciprocal transcriptional response.BMC genomics · 2016Article
- Relationship of disease-associated gene expression to cardiac phenotype is buffered by genetic diversity and chromatin regulation.Physiological genomics · 2016Article
- Assessing Cardiac Metabolism: A Scientific Statement From the American Heart Association.Circulation research · 2016Review
- GDF11 does not rescue aging-related pathological hypertrophy.Circulation research · 2015Article
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
rationaleThe extent of heart disease varies from person to person, suggesting that genetic background is important in pathology. Genetic background is also important when selecting appropriate mouse models to study heart disease. This study examines heart growth as a function of strain, specifically C57BL/6 and DBA/2 mouse strains.
objectiveIn this study, we test the hypothesis that two strains of mice, C57BL/6 and DBA/2, will produce varying degrees of heart growth in both physiological and pathological settings. METHODS AND
resultsDifferences in heart dimensions are detectable by echocardiography at 8 weeks of age. Percentages of cardiac progenitor cells (c-kit+ cells) and mononucleated cells were found to be in a higher percentage in DBA/2 mice, and more tri- and quad-nucleated cells were in C57BL/6 mice. Cardiomyocyte turnover shows no significant changes in mitotic activity, however, there is more apoptotic activity in DBA/2 mice. Cardiomyocyte cell size increased with age, but increased more in DBA/2 mice, although percentages of nucleated cells remained the same in both strains. Two-week isoproterenol stimulation showed an increase in heart growth in DBA/2 mice, both at cardiomyocyte and whole heart level. In isoproterenol-treated DBA/2 mice, there was also a greater expression level of the hypertrophy marker, ANF, compared to C57BL/6 mice.
conclusionWe conclude that the DBA/2 mouse strain has a more immature cardiac phenotype, which correlates to a cardiac protective response to hypertrophy in both physiological and pathological stimulations.
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Registered trials
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