ArticleThe Journal of clinical investigation1999
Beta-adrenergic receptor blockade arrests myocyte damage and preserves cardiac function in the transgenic G(salpha) mouse.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 120 citations in OpenAlex.
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- Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice.The journal of physiological sciences : JPS · 2023Article
- Ablation of CXCR4 expression in cardiomyocytes exacerbates isoproterenol‑induced cell death and heart failure.International journal of molecular medicine · 2023Article
- Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts.Biology · 2022Review
- Effects of Propranolol on Bone, White Adipose Tissue, and Bone Marrow Adipose Tissue in Mice Housed at Room Temperature or Thermoneutral Temperature.Frontiers in endocrinology · 2020Article
- Regulator of G Protein Signaling 6 Protects the Heart from Ischemic Injury.The Journal of pharmacology and experimental therapeutics · 2017Article
- Cardiac Effects of Attenuating Gsα - Dependent Signaling.PloS one · 2016Article
- Article
- Effects of anesthesia on conventional and speckle tracking echocardiographic parameters in a mouse model of pressure overload.Experimental and therapeutic medicine · 2015Article
- Effects of GRK5 and ADRB1 polymorphisms influence on systolic heart failure.Journal of translational medicine · 2015Article
- AT1 receptor antagonism to reduce aortic expansion in Marfan syndrome: lost in translation or in need of different interpretation?Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Epac1-dependent phospholamban phosphorylation mediates the cardiac response to stresses.The Journal of clinical investigation · 2014Article
- GNAS gene variants affect β-blocker-related survival after coronary artery bypass grafting.Anesthesiology · 2014Observational
- β1-Adrenergic receptor blockade extends the life span of Drosophila and long-lived mice.Age (Dordrecht, Netherlands) · 2013Article
- Adenylyl cyclase type 5 in cardiac disease, metabolism, and aging.American journal of physiology. Heart and circulatory physiology · 2013Review
- Cardiomyocyte life-death decisions in response to chronic β-adrenergic signaling.Circulation research · 2013Article
- Propranolol enhances cell cycle-related gene expression in pressure overloaded hearts.British journal of pharmacology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transgenic (TG) mice with cardiac G(salpha) overexpression exhibit enhanced inotropic and chronotropic responses to sympathetic stimulation, but develop cardiomyopathy with age. We tested the hypothesis that cardiomyopathy in TG mice with G(salpha) overexpression could be averted with chronic beta-adrenergic receptor (beta-AR) blockade. TG mice and age-matched wild-type littermates were treated with the beta-AR blocker propranolol for 6-7 months, starting at a time when the cardiomyopathy was developing but was not yet severe enough to induce significant cardiac depression (9.5 months of age), and ending at a time when cardiac depression and cardiomyopathy would have been clearly manifest (16 months of age). Propranolol treatment, which can induce cardiac depression in the normal heart, actually prevented cardiac dilation and the depressed left ventricular function characteristic of older TG mice, and abolished premature mortality. Propranolol also prevented the increase in myocyte cross-sectional area and myocardial fibrosis. Myocyte apoptosis, already apparent in 9-month-old TG mice, was actually eliminated by chronic propranolol. This study indicates that chronic sympathetic stimulation over an extended period is deleterious and results in cardiomyopathy. Conversely, beta-AR blockade is salutary in this situation and can prevent the development of cardiomyopathy.
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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.