ReviewMolecular medicine (Cambridge, Mass.)2012
Signaling to cardiac hypertrophy: insights from human and mouse RASopathies.
Review in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 49 citations in OpenAlex.
- Selected Pathway Analyses to Gain Mechanistic Insights into the Pathogenesis of Feline Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2025Article
- Signalling pathways involved in urotensin II induced ventricular myocyte hypertrophy.PloS one · 2025Article
- RASopathies and Cardiac Complications: Insights into Mechanisms, Diagnosis, and Innovative Treatments.Current cardiology reviews · 2025Review
- Local adaptation, plasticity, and evolved resistance to hypoxic cold stress in high-altitude deer mice.bioRxiv : the preprint server for biology · 2024Article
- Novel Multiplexed Plasma Biomarker Panel Has Diagnostic and Prognostic Potential in Children With Hypertrophic Cardiomyopathy.Circulation. Genomic and precision medicine · 2024Article
- To Repair a Broken Heart: Stem Cells in Ischemic Heart Disease.Current issues in molecular biology · 2024Review
- An Assessment of the Therapeutic Landscape for the Treatment of Heart Disease in the RASopathies.Cardiovascular drugs and therapy · 2023Review
- Sigma-1 Receptor Signaling: In Search of New Therapeutic Alternatives for Cardiovascular and Renal Diseases.International journal of molecular sciences · 2023Review
- What Causes Hypertrophic Cardiomyopathy?The American journal of cardiology · 2022Review
- Hsa_circ_0003748 promotes disease progression in rheumatic valvular heart disease by sponging miR-577.Journal of clinical laboratory analysis · 2022Article
- HRas and Myc synergistically induce cell cycle progression and apoptosis of murine cardiomyocytes.Frontiers in cardiovascular medicine · 2022Article
- Inside the Noonan "universe": Literature review on growth, GH/IGF axis and rhGH treatment: Facts and concerns.Frontiers in endocrinology · 2022Review
- Molecules linked to Ras signaling as therapeutic targets in cardiac pathologies.Biological research · 2021Review
- Lysosomal-Associated Protein Transmembrane 5 Functions as a Novel Negative Regulator of Pathological Cardiac Hypertrophy.Frontiers in cardiovascular medicine · 2021Article
- Interference with ERK-dimerization at the nucleocytosolic interface targets pathological ERK1/2 signaling without cardiotoxic side-effects.Nature communications · 2020Article
- Cardiac Myxoma in a Patient With Hypertrophic Cardiomyopathy.JACC. Case reports · 2020Article
- How to Steer and Control ERK and the ERK Signaling Cascade Exemplified by Looking at Cardiac Insufficiency.International journal of molecular sciences · 2019Article
- ERK: A Key Player in the Pathophysiology of Cardiac Hypertrophy.International journal of molecular sciences · 2019Review
- A severe clinical phenotype of Noonan syndrome with neonatal hypertrophic cardiomyopathy in the second case worldwide with RAF1 S259Y neomutation.Genetics research · 2019Article
- Chronic kidney disease induces left ventricular overexpression of the pro-hypertrophic microRNA-212.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state. An integral part of the pathogenesis of the hypertrophic cardiomyopathy disease (HCM) is the activation of the rat sarcoma (RAS)/RAF/MEK (mitogen-activated protein kinase kinase)/MAPK (mitogen-activated protein kinase) cascade. Therefore, the molecular signaling involving RAS has been the subject of intense research efforts, particularly after the identification of the RASopathies. These constitute a class of developmental disorders caused by germline mutations affecting proteins contributing to the RAS pathway. Among other phenotypic features, a subset of these syndromes is characterized by HCM, prompting researchers and clinicians to delve into the chief signaling constituents of cardiac hypertrophy. In this review, we summarize current advances in the knowledge of the molecular signaling events involved in the pathogenesis of cardiac hypertrophy through work completed on patients and on genetically manipulated animals with HCM and RASopathies. Important insights are drawn from the recognition of parallels between cardiac hypertrophy and cancer. Future research promises to further elucidate the complex molecular interactions responsible for cardiac hypertrophy, possibly pointing the way for the identification of new specific targets for the treatment of HCM.
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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.