ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Cardiac pressure overload hypertrophy is differentially regulated by β-adrenergic receptor subtypes.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Morphometric and Molecular Interplay in Hypertension-Induced Cardiac Remodeling with an Emphasis on the Potential Therapeutic Implications.International journal of molecular sciences · 2025Review
- Fluoxetine promotes IL-10-dependent metabolic defenses to protect from sepsis-induced lethality.Science advances · 2025Article
- USP20 deletion promotes eccentric cardiac remodeling in response to pressure overload and increases mortality.American journal of physiology. Heart and circulatory physiology · 2024Article
- Internalized β2-Adrenergic Receptors Oppose PLC-Dependent Hypertrophic Signaling.Circulation research · 2024Article
- Transcriptomics data integration and analysis to uncover hallmark genes in hypertrophic cardiomyopathy.American journal of translational research · 2024Article
- New drug discovery of cardiac anti-arrhythmic drugs: insights in animal models.Scientific reports · 2023Article
- A non-coding GWAS variant impacts anthracycline-induced cardiotoxic phenotypes in human iPSC-derived cardiomyocytes.Nature communications · 2022Article
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
- Dysfunctional Network and Mutation Genes of Hypertrophic Cardiomyopathy.Journal of healthcare engineering · 2022Article
- Dysfunctional network of hub genes in hypertrophic cardiomyopathy patients.American journal of translational research · 2022Article
- Changes in Cardiac Function During the Development of Uremic Cardiomyopathy and the Effect of Salvianolic Acid B Administration in a Rat Model.Frontiers in veterinary science · 2022Article
- Context-specific network modeling identifies new crosstalk in β-adrenergic cardiac hypertrophy.PLoS computational biology · 2020Article
- Article
- Accurate assessment of LV function using the first automated 2D-border detection algorithm for small animals - evaluation and application to models of LV dysfunction.Cardiovascular ultrasound · 2019Article
- Myofibroblast β2 adrenergic signaling amplifies cardiac hypertrophy in mice.Biochemical and biophysical research communications · 2019Article
- The deubiquitinase ubiquitin-specific protease 20 is a positive modulator of myocardial βThe Journal of biological chemistry · 2019Article
- Evaluation of a commercial multi-dimensional echocardiography technique for ventricular volumetry in small animals.Cardiovascular ultrasound · 2018Article
- A Potential Link Between Oxidative Stress and Endothelial-to-Mesenchymal Transition in Systemic Sclerosis.Frontiers in immunology · 2018Review
- Molecular Mechanisms of Right Ventricular Failure.Circulation · 2015Review
- Deletion of CXCR4 in cardiomyocytes exacerbates cardiac dysfunction following isoproterenol administration.Gene therapy · 2014Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
In isolated myocytes, hypertrophy induced by norepinephrine is mediated via α(1)-adrenergic receptors (ARs) and not β-ARs. However, mice with deletions of both major cardiac α(1)-ARs still develop hypertrophy in response to pressure overload. Our purpose was to better define the role of β-AR subtypes in regulating cardiac hypertrophy in vivo, important given the widespread clinical use of β-AR antagonists and the likelihood that patients treated with these agents could develop conditions of further afterload stress. Mice with deletions of β(1), β(2), or both β(1)- and β(2)-ARs were subjected to transverse aortic constriction (TAC). After 3 wk, β(1)(-/-) showed a 21% increase in heart to body weight vs. sham controls, similar to wild type, whereas β(2)(-/-) developed exaggerated (49% increase) hypertrophy. Only when both β-ARs were ablated (β(1)β(2)(-/-)) was hypertrophy totally abolished. Cardiac function was preserved in all genotypes. Several known inhibitors of cardiac hypertrophy (FK506 binding protein 5, thioredoxin interacting protein, and S100A9) were upregulated in β(1)β(2)(-/-) compared with the other genotypes, whereas transforming growth factor-β(2), a positive mediator of hypertrophy was upregulated in all genotypes except the β(1)β(2)(-/-). In contrast to recent reports suggesting that angiogenesis plays a critical role in regulating cardiac hypertrophy-induced heart failure, we found no evidence that angiogenesis or its regulators (VEGF, Hif1α, and p53) play a role in compensated cardiac hypertrophy. Pressure overload hypertrophy in vivo is dependent on a coordination of signaling through both β(1)- and β(2)-ARs, mediated through several key cardiac remodeling pathways. Angiogenesis is not a prerequisite for compensated cardiac hypertrophy.
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