ArticleJournal of molecular and cellular cardiology2012
Beta1-adrenergic receptors promote focal adhesion signaling downregulation and myocyte apoptosis in acute volume overload.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Multiscale model calibrated with a Bayesian algorithm predicts long-term outcomes of treatments for mitral valve regurgitation in animal models.Biomechanics and modeling in mechanobiology · 2026Article
- The beta1-adrenergic receptor in the heart.Cell death discovery · 2025Review
- Contributions of mechanical loading and hormonal changes to eccentric hypertrophy during volume overload: A Bayesian analysis using logic-based network models.PLoS computational biology · 2025Article
- Downregulation of PTEN Promotes AutophagyFrontiers in cardiovascular medicine · 2022Article
- Clinical value of detecting autoantibodies against βJournal of geriatric cardiology : JGC · 2020Article
- Multifunctional Role of Chymase in Acute and Chronic Tissue Injury and Remodeling.Circulation research · 2018Review
- Mesenchymal stem cell conditioned medium alleviates oxidative stress injury induced by hydrogen peroxide via regulating miR143 and its target protein in hepatocytes.BMC immunology · 2017Article
- Effect of chronic pretreatment with beta-blockers on no-reflow phenomenon in diabetic patients with acute ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2017Article
- Exposure to chronic alcohol accelerates development of wall stress and eccentric remodeling in rats with volume overload.Journal of molecular and cellular cardiology · 2016Article
- Increased fibroblast chymase production mediates procollagen autophagic digestion in volume overload.Journal of molecular and cellular cardiology · 2016Article
- Signaling Pathways in Cardiac Myocyte Apoptosis.BioMed research international · 2016Review
- Mechanical Stretch Inhibits MicroRNA499 via p53 to Regulate Calcineurin-A Expression in Rat Cardiomyocytes.PloS one · 2016Article
- Stimulating endogenous cardiac repair.Frontiers in cell and developmental biology · 2015Review
- The multiple mechanistic faces of a pure volume overload: implications for therapy.The American journal of the medical sciences · 2014Review
- Focal adhesion signaling in heart failure.Pflugers Archiv : European journal of physiology · 2014Review
- Myofilament dysfunction as an emerging mechanism of volume overload heart failure.Pflugers Archiv : European journal of physiology · 2014Review
- CapZ and actin capping dynamics increase in myocytes after a bout of exercise and abates in hours after stimulation ends.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Effect of metoprolol on myocardial apoptosis after coronary microembolization in rats.World journal of emergency medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Numerous studies demonstrated increased expression of extracellular matrix (ECM) proteins and activation of focal adhesion (FA) signaling pathways in models of pressure overload-induced cardiac hypertrophy. However, little is known about FA signaling in response to volume overload where cardiac hypertrophy is associated with ECM loss. This study examines the role of beta1-adrenergic receptors (β(1)-ARs) in FA signaling changes and myocyte apoptosis induced during acute hemodynamic stress of volume overload. Rats with eccentric cardiac hypertrophy induced after aorto-caval fistula (ACF) develop reduced interstitial collagen content and decreased tyrosine phosphorylation of key FA signaling molecules FAK, Pyk(2) and paxillin along with an increase in cardiac myocyte apoptosis. ACF also increased activation of PTEN, a dual lipid and protein phosphatase, and its interaction with FA proteins. β(1)-AR blockade (extended-release of metoprolol succinate, 100mg QD) markedly attenuated PTEN activation, restored FA signaling and reduced myocyte apoptosis induced by ACF at 2days, but failed to reduce interstitial collagen loss and left ventricular dilatation. Treating cultured myocytes with β(1)-AR agonists or adenoviral expression of β(1)-ARs caused PTEN activation and interaction with FA proteins, thus leading to FA signaling downregulation and myocyte apoptosis. Adenoviral-mediated expression of a catalytically inactive PTEN mutant or wild-type FAK restored FA signaling downregulation and attenuated myocyte apoptosis induced by β(1)-ARs. Collectively, these data show that β(1)-AR stimulation in response to ACF induces FA signaling downregulation through an ECM-independent mechanism. This effect involves PTEN activation and may contribute to adverse cardiac remodeling and function in the course of volume overload.
Indexed as
Identifiers
What OpenQuestion holds
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.