ArticleJournal of molecular and cellular cardiology2014
β-Arrestins regulate human cardiac fibroblast transformation and collagen synthesis in adverse ventricular remodeling.
Article in Journal of molecular and cellular cardiology, 2014. 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, 36 citations in OpenAlex.
- Cell-Specific Signal Bias Shapes β3-Adrenoceptor Profibrotic Activation in Cardiac Fibroblasts.Journal of cellular and molecular medicine · 2026Article
- Challenges and opportunities for ginseng-based medicines in treating cardiac fibrosis from mechanistic insights to clinical translation.Chinese herbal medicines · 2026Review
- β-arrestin2: an emerging player and potential therapeutic target in inflammatory immune diseases.Acta pharmacologica Sinica · 2025Review
- Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions.Heliyon · 2024Review
- A Review of Therapeutic Strategies against Cardiac Fibrosis: From Classical Pharmacology to Novel Molecular, Epigenetic, and Biotechnological Approaches.Reviews in cardiovascular medicine · 2023Review
- Chronic activation of human cardiac fibroblasts in vitro attenuates the reversibility of the myofibroblast phenotype.Scientific reports · 2023Article
- Review
- Therapeutic targets for cardiac fibrosis: from old school to next-gen.The Journal of clinical investigation · 2022Review
- Sympatho-adrenergic mechanisms in heart failure: new insights into pathophysiology.Medical review (2021) · 2021Article
- AMPKα1 deletion in myofibroblasts exacerbates post-myocardial infarction fibrosis by a connexin 43 mechanism.Basic research in cardiology · 2021Article
- Complex Relationship Between Cardiac Fibroblasts and Cardiomyocytes in Health and Disease.Journal of the American Heart Association · 2021Review
- β-Arrestin2 is increased in liver fibrosis in humans and rodents.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- miR-29b-3p inhibits post-infarct cardiac fibrosis by targeting FOS.Bioscience reports · 2020Article
- Mechanisms of cardiac collagen deposition in experimental models and human disease.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Not all arrestins are created equal: Therapeutic implications of the functional diversity of the β-arrestins in the heart.World journal of cardiology · 2019Article
- Regulation of cardiac fibroblast-mediated maladaptive ventricular remodeling by β-arrestins.PloS one · 2019Article
- Changes in cardiac resident fibroblast physiology and phenotype in aging.American journal of physiology. Heart and circulatory physiology · 2018Review
- TAK-272 (imarikiren), a novel renin inhibitor, improves cardiac remodeling and mortality in a murine heart failure model.PloS one · 2018Article
- Pharmacological and Activated Fibroblast Targeting of Gβγ-GRK2 After Myocardial Ischemia Attenuates Heart Failure Progression.Journal of the American College of Cardiology · 2017Article
- Thrombospondins: A Role in Cardiovascular Disease.International journal of molecular sciences · 2017Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac fibroblasts (CFs) produce and degrade the myocardial extracellular matrix and are critical in maladaptive ventricular remodeling that can result in heart failure (HF). β-Arrestins are important signaling molecules involved in β-adrenergic receptor (β-AR) desensitization and can also mediate signaling in a G protein-independent fashion. We hypothesize that β-arrestins play an important role in the regulation of adult human CF biology with regard to myofibroblast transformation, increased collagen synthesis, and myocardial fibrosis which are important in the development of HF. β-Arrestin1 & 2 expression is significantly upregulated in adult human CF isolated from failing left ventricles and β-AR signaling is uncoupled with loss of β-agonist-mediated inhibition of collagen synthesis versus normal control CF. Knockdown of either β-arrestin1 or 2 restored β-AR signaling and β-agonist mediated inhibition of collagen synthesis. Overexpression of β-arrestins in normal CF led to a failing phenotype with increased baseline collagen synthesis, impaired β-AR signaling, and loss of β-agonist-mediated inhibition of collagen synthesis. β-Arrestin knockdown in failing CF diminished TGF-β stimulated collagen synthesis and also inhibited ERK phosphorylation. Overexpression of β-arrestins in normal CF increased basal ERK1/2 and Smad2/3 phosphorylation and enhanced TGF-β-stimulated collagen synthesis. This was prevented by pre-treatment with a MEK1/2 inhibitor. Enhanced β-arrestin signaling appears to be deleterious in CF by promoting a pro-fibrotic phenotype via uncoupling of β-AR signaling as well as potentiating ERK and Smad signaling. Targeted inhibition of β-arrestins in CF may represent a therapeutic strategy to prevent maladaptive myocardial fibrosis.
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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.