ReviewOncogene2001
G-proteins in growth and apoptosis: lessons from the heart.
Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 122 citations in OpenAlex.
- Cardiomyocyte-specific overexpression of GPR22 ameliorates cardiac injury in mice with acute myocardial infarction.BMC cardiovascular disorders · 2024Article
- Ablation of CXCR4 expression in cardiomyocytes exacerbates isoproterenol‑induced cell death and heart failure.International journal of molecular medicine · 2023Article
- GqPCR-stimulated dephosphorylation of AKT is induced by an IGBP1-mediated PP2A switch.Cell communication and signaling : CCS · 2022Article
- Identification of hub genes in chronically hypoxic myocardium using bioinformatics analysis.Molecular medicine reports · 2019Article
- Influence of the plasminogen activator system on necrosis in acute myocardial infarction: analysis of urokinase- and urokinase receptor-knockout mouse models.American journal of translational research · 2019Article
- Mechanical stretch induced transcriptomic profiles in cardiac myocytes.Scientific reports · 2018Article
- Heart failure with preserved ejection fraction and skeletal muscle physiology.Heart failure reviews · 2017Review
- Selective coupling of the S1PJournal of molecular and cellular cardiology · 2017Article
- Activation of HuR downstream of p38 MAPK promotes cardiomyocyte hypertrophy.Cellular signalling · 2016Article
- Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway.PloS one · 2015Article
- A new non-canonical pathway of Gα(q) protein regulating mitochondrial dynamics and bioenergetics.Cellular signalling · 2014Article
- Protection of cardiomyocytes from the hypoxia-mediated injury by a peptide targeting the activator of G-protein signaling 8.PloS one · 2014Article
- Cardiac alpha1-adrenergic receptors: novel aspects of expression, signaling mechanisms, physiologic function, and clinical importance.Pharmacological reviews · 2014Review
- A novel immunomodulator, FTY-720 reverses existing cardiac hypertrophy and fibrosis from pressure overload by targeting NFAT (nuclear factor of activated T-cells) signaling and periostin.Circulation. Heart failure · 2013Article
- Systemic revealing pharmacological signalling pathway networks in the hippocampus of ischaemia-reperfusion mice treated with baicalin.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- β-adrenoceptor regulates miRNA expression in rat heart.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
- Gq protein-induced apoptosis is mediated by AKT kinase inhibition that leads to protein kinase C-induced c-Jun N-terminal kinase activation.The Journal of biological chemistry · 2011Article
- β-Cell Specific Overexpression of GPR39 Protects against Streptozotocin-Induced Hyperglycemia.International journal of endocrinology · 2011Article
- Revisited and revised: is RhoA always a villain in cardiac pathophysiology?Journal of cardiovascular translational research · 2010Review
- The Rho guanine nucleotide exchange factor AKAP13 (BRX) is essential for cardiac development in mice.The Journal of biological chemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The acute contractile function of the heart is controlled by the effects of released nonepinephrine (NE) on cardiac adrenergic receptors. NE can also act in a more chronic fashion to induce cardiomyocyte growth, characterized by cell enlargement (hypertrophy), increased protein synthesis, alterations in gene expression and addition of sarcomeres. These responses enhance cardiomyocyte contractile function and thus allow the heart to compensate for increased stress. The hypertrophic effects of NE are mediated through Gq-coupled alpha(1)-adrenergic receptors and are mimicked by the actions of other neurohormones (endothelin, prostaglandin F(2alpha) angiotensin II) that also act on Gq-coupled receptors. Activation of phospholipase C by Gq is necessary for these responses, and protein kinase C and MAP kinases have also been implicated. Gq stimulated cardiac hypertrophy is also evident in transgenic mouse models. In contrast, stimulation of G(s)-coupled beta-adrenergic receptors or G(i)-coupled receptors do not directly effect cardiomyocyte hypertrophy. Apoptosis is also induced by G-protein-coupled receptor stimulation in cardiomyocytes. Sustained or excessive activation of either Gq- or Gs-signaling pathways results in apoptotic loss of cardiomyocytes both in vitro and in vivo. Apoptosis is associated with decreased ventricular function in the failing heart. Cardiomyocytes provide an ideal model system for understanding the basis for G-protein mediated hypertrophy and apoptosis, and the mechanisms responsible for the transition from compensatory to deleterious levels of signaling. This information may prove critical for designing interventions that prevent the pathophysiological consequences of heart failure.
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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.