ArticleCirculation2005
AFos dissociates cardiac myocyte hypertrophy and expression of the pathological gene program.
Article in Circulation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Nanoparticle-Based Therapeutic Strategies for Pathological Cardiac Hypertrophy: Preclinical Advances, Translational Challenges, and Future Perspectives.International journal of nanomedicine · 2026Review
- Chemogenetic neuronal silencing decouples c-Jun activation from cell death in the temporal cortex.The European journal of neuroscience · 2024Article
- Upregulation of Phospholipase C Gene Expression Due to Norepinephrine-Induced Hypertrophic Response.Cells · 2022Review
- Dihydroartemisinin beneficially regulates splenic immune cell heterogeneity through the SOD3-JNK-AP-1 axis.Science China. Life sciences · 2022Article
- Stem cell-derived extracellular vesicles reduce the expression of molecules involved in cardiac hypertrophy-In a model of human-induced pluripotent stem cell-derived cardiomyocytes.Frontiers in pharmacology · 2022Article
- Resistin-Like Molecule α Dysregulates Cardiac Bioenergetics in Neonatal Rat Cardiomyocytes.Frontiers in cardiovascular medicine · 2021Article
- A Novel Method of Isolating Myofibrils From Primary Cardiomyocyte Culture Suitable for Myofibril Mechanical Study.Frontiers in cardiovascular medicine · 2019Article
- Activin Receptor-Like Kinase 4 Haplodeficiency Mitigates Arrhythmogenic Atrial Remodeling and Vulnerability to Atrial Fibrillation in Cardiac Pathological Hypertrophy.Journal of the American Heart Association · 2018Article
- Network-based predictions of in vivo cardiac hypertrophy.Journal of molecular and cellular cardiology · 2018Article
- Gallic acid prevents isoproterenol-induced cardiac hypertrophy and fibrosis through regulation of JNK2 signaling and Smad3 binding activity.Scientific reports · 2016Article
- MAP kinase kinase kinase-2 (MEKK2) regulates hypertrophic remodeling of the right ventricle in hypoxia-induced pulmonary hypertension.American journal of physiology. Heart and circulatory physiology · 2013Article
- Cross-talk between angiotensin II and IGF-1-induced connexin 43 expression in human saphenous vein smooth muscle cells.Journal of cellular and molecular medicine · 2011Article
- Sex differences in cardiomyocyte connexin43 expression.Journal of cardiovascular pharmacology · 2011Article
- AFos inhibits phenylephrine-mediated contractile dysfunction by altering phospholamban phosphorylation.American journal of physiology. Heart and circulatory physiology · 2010Article
- Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway.Journal of molecular and cellular cardiology · 2008Article
- Knockout of beta(1)- and beta(2)-adrenoceptors attenuates pressure overload-induced cardiac hypertrophy and fibrosis.British journal of pharmacology · 2008Article
- Propranolol causes a paradoxical enhancement of cardiomyocyte foetal gene response to hypertrophic stimuli.British journal of pharmacology · 2007Article
- Divergence of hypertrophic growth and fetal gene profile: the influence of beta-blockers.British journal of pharmacology · 2007Article
- TrpC3 regulates hypertrophy-associated gene expression without affecting myocyte beating or cell size.PloS one · 2007Article
- Repression of anti-apoptotic genes via AP-1 as a mechanism of apoptosis induction in ventricular cardiomyocytes.Pflugers Archiv : European journal of physiology · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundAlthough induction of activator protein-1 (AP-1) transcription factor activity has been observed in cardiac hypertrophy, a direct role for AP-1 in myocardial growth and gene expression remains obscure. METHODS AND
resultsHypertrophy was induced in cultured neonatal rat cardiomyocytes with phenylephrine or overexpression of a constitutively active MAP3K, MKK6. In both treatment groups, induction of the pathological gene profile was observed, ie, expression of beta-myosin heavy chain (betaMHC), atrial/brain natriuretic peptides (ANP/BNP), and skeletal alpha-actin (sACT) was increased, whereas expression for alpha-myosin heavy chain (alphaMHC) and the sarcoplasmic reticulum Ca2+-ATPase (SERCA) genes was repressed. The role of AP-1 in the hypertrophic phenotype was evaluated with the use of an adenoviral construct expressing a dominant negative mutant of the c-Fos proto-oncogene (AdAFos). Although AFos did not change the myocyte growth response, it abrogated the gene profile to both agonists, including the upregulation of both alphaMHC and SERCA expression.
conclusionsAlthough c-Fos/AP-1 is necessary for induction of the pathological/fetal gene program, it does not appear to be critical for cardiomyocyte hypertrophy.
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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.