ArticleCirculation. Cardiovascular genetics2015
Mapping genetic contributions to cardiac pathology induced by Beta-adrenergic stimulation in mice.
Article in Circulation. Cardiovascular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 92 citations in OpenAlex.
- Article
- Integration of Collaborative Cross and Hybrid Mouse Diversity Panel studies does not significantly improve genome wide association study results.BMC research notes · 2026Article
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- Genetic background is associated with distinct patterns of proarrhythmogenic remodeling leading to atrial fibrillation in pigs with ischemic heart failure.Basic research in cardiology · 2026Article
- Genetic determinants of heart failure susceptibility and response in the collaborative cross mouse population.Genetics · 2026Article
- A systems genetics approach to uncover mitochondrial drivers of heart failure reveals mitochondria-nuclear cross talk in genetically diverse mouse strains.bioRxiv : the preprint server for biology · 2025Article
- Mapping DNA methylation to cardiac pathologies induced by beta-adrenergic stimulation in a large panel of mice.Epigenetics · 2025Article
- Loss of Elmsan1 in cardiomyocytes leads to age-dependent cardiac dysfunction and reduced lifespan.American journal of physiology. Heart and circulatory physiology · 2025Article
- Echocardiographic Assessment of Cardiac Function in Mouse Models of Heart Disease.International journal of molecular sciences · 2025Review
- Collagen V regulates renal function after kidney injury and can be pharmacologically targeted to enhance kidney repair in mice.Science translational medicine · 2025Article
- The multifaceted role of mitochondria in cardiac function: insights and approaches.Cell communication and signaling : CCS · 2024Review
- Rapid onset fibrotic remodeling and ventricular dysfunction induced by phenylephrine involve targeted reprogramming of myocyte and fibroblast transcriptomes.bioRxiv : the preprint server for biology · 2024Article
- The Purinergic Nature of Pseudoxanthoma Elasticum.Biology · 2024Review
- Isoproterenol induced cardiac hypertrophy: A comparison of three doses and two delivery methods in C57BL/6J mice.PloS one · 2024Article
- Histone H1.0 couples cellular mechanical behaviors to chromatin structure.Nature cardiovascular research · 2024Article
- Gene Regulatory Networks in Coronary Artery Disease.Current atherosclerosis reports · 2023Review
- Systems genetics approaches for understanding complex traits with relevance for human disease.eLife · 2023Review
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- Regression of cardiac hypertrophy in health and disease: mechanisms and therapeutic potential.Nature reviews. Cardiology · 2023Review
- Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundChronic stress-induced cardiac pathology exhibits both a wide range in severity and a high degree of heterogeneity in clinical manifestation in human patients. This variability is contributed to by complex genetic and environmental etiologies within the human population. Genetic approaches to elucidate the genetics underlying the acquired forms of cardiomyopathies, including genome-wide association studies, have been largely unsuccessful, resulting in limited knowledge as to the contribution of genetic variations for this important disease. METHODS AND
resultsUsing the β-adrenergic agonist isoproterenol as a specific pathological stressor to circumvent the problem of etiologic heterogeneity, we performed a genome-wide association study for genes influencing cardiac hypertrophy and fibrosis in a large panel of inbred mice. Our analyses revealed 7 significant loci and 17 suggestive loci, containing an average of 14 genes, affecting cardiac hypertrophy, fibrosis, and surrogate traits relevant to heart failure. Several loci contained candidate genes which are known to contribute to Mendelian cardiomyopathies in humans or have established roles in cardiac pathology based on molecular or genetic studies in mouse models. In particular, we identify Abcc6 as a novel gene underlying a fibrosis locus by validating that an allele with a splice mutation of Abcc6 dramatically and rapidly promotes isoproterenol-induced cardiac fibrosis.
conclusionsGenetic variants significantly contribute to the phenotypic heterogeneity of stress-induced cardiomyopathy. Systems genetics is an effective approach to identify genes and pathways underlying the specific pathological features of cardiomyopathies. Abcc6 is a previously unrecognized player in the development of stress-induced cardiac fibrosis.
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