ArticleCirculation research2009
Cardiomyocyte-specific loss of neurofibromin promotes cardiac hypertrophy and dysfunction.
Article in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Cardiac Monitoring for Patients Undergoing Treatment With MEK Inhibitor Monotherapy.Current oncology reports · 2026Review
- NF1 with Multiple Cardiac Structural Abnormalities Leading to Cerebral Infarction.Diagnostics (Basel, Switzerland) · 2026Article
- AlkCell communication and signaling : CCS · 2025Article
- RICH1 is a novel key suppressor of isoproterenol‑ or angiotensin II‑induced cardiomyocyte hypertrophy.Molecular medicine reports · 2024Article
- An Assessment of the Therapeutic Landscape for the Treatment of Heart Disease in the RASopathies.Cardiovascular drugs and therapy · 2023Review
- Substantial impact of 3-iodothyronamine (T1AM) on the regulations of fluorescent thermoprobe-measured cellular temperature and natriuretic peptide expression in cardiomyocytes.Scientific reports · 2022Article
- Roles of transient receptor potential channel 6 in glucose-induced cardiomyocyte injury.World journal of diabetes · 2022Article
- Generation and characterization of a Myh6-driven Cre knockin mouse line.Transgenic research · 2021Article
- Molecules linked to Ras signaling as therapeutic targets in cardiac pathologies.Biological research · 2021Review
- Generation of Transgenic Mice that Conditionally Overexpress Tenascin-C.Frontiers in immunology · 2021Article
- Identifying the key regulators that promote cell-cycle activity in the hearts of early neonatal pigs after myocardial injury.PloS one · 2020Article
- Prevalence, Type, and Molecular Spectrum ofGenes · 2019Article
- Myeloid Cell mPges-1 Deletion Attenuates Mortality Without Affecting Remodeling After Acute Myocardial Infarction in Mice.The Journal of pharmacology and experimental therapeutics · 2019Article
- SCN5A Nonsense Mutation and NF1 Frameshift Mutation in a Family With Brugada Syndrome and Neurofibromatosis.Frontiers in genetics · 2019Article
- Emerging genotype-phenotype relationships in patients with large NF1 deletions.Human genetics · 2017Review
- Inhibition of farnesyl pyrophosphate synthase improves pressure overload induced chronic cardiac remodeling.Scientific reports · 2016Article
- Targeting NF2-Hippo/Yap signaling pathway for cardioprotection after ischemia/reperfusion injury.Annals of translational medicine · 2016Article
- RSK3 is required for concentric myocyte hypertrophy in an activated Raf1 model for Noonan syndrome.Journal of molecular and cellular cardiology · 2016Article
- Neurofibromatosis 1-associated panhypopituitarism presenting as hypoglycaemic seizures and stroke-like symptoms.BMJ case reports · 2015Article
- RASopathies: unraveling mechanisms with animal models.Disease models & mechanisms · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
rationaleNeurofibromatosis type 1 (NF1) is a common autosomal dominant disorder with a broad array of clinical manifestations, including benign and malignant tumors, and characteristic cutaneous findings. NF1 patients also have an increased incidence of cardiovascular diseases, including obstructive vascular disorders and hypertension. The disease gene, NF1, encodes neurofibromin, a ubiquitously expressed protein that acts, in part, as a Ras-GAP (GTP-ase activating protein), downregulating the activity of activated Ras protooncogenes. In animal models, endothelial and smooth muscle expression of the disease gene is critical for normal heart development and the prevention of vascular disease, respectively.
objectiveTo determine the role of NF1 in the postnatal and adult heart. METHODS AND
resultsWe generated mice with homozygous loss of the murine homolog Nf1 in myocardium (Nf1mKO) and evaluated their hearts for biochemical, structural, and functional changes. Nf1mKO mice have normal embryonic cardiovascular development but have marked cardiac hypertrophy, progressive cardiomyopathy, and fibrosis in the adult. Hyperactivation of Ras and downstream pathways are seen in the heart with the loss of Nf1, along with activation of a fetal gene program.
conclusionsThis report describes a critical role of Nf1 in the regulation of cardiac growth and function. Activation of pathways known to be involved in cardiac hypertrophy and dysfunction are seen with the loss of myocardial neurofibromin.
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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.