ArticleProceedings of the National Academy of Sciences of the United States of America1997
Ras-dependent pathways induce obstructive hypertrophy in echo-selected transgenic mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 65 citations in OpenAlex.
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- RASopathies and Cardiac Complications: Insights into Mechanisms, Diagnosis, and Innovative Treatments.Current cardiology reviews · 2025Review
- Prediction of Major Adverse Cardiovascular Events in Patients With Hypertrophic Cardiomyopathy Using Proteomics Profiling.Circulation. Genomic and precision medicine · 2022Article
- HRAS germline mutations impair LKB1/AMPK signaling and mitochondrial homeostasis in Costello syndrome models.The Journal of clinical investigation · 2022Article
- Molecules linked to Ras signaling as therapeutic targets in cardiac pathologies.Biological research · 2021Review
- Network-based predictions of in vivo cardiac hypertrophy.Journal of molecular and cellular cardiology · 2018Article
- Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research.Molecular and cellular biochemistry · 2017Review
- Dominant negative Ras attenuates pathological ventricular remodeling in pressure overload cardiac hypertrophy.Biochimica et biophysica acta · 2015Article
- Proteomic profiling of H-Ras-G12V induced hypertrophic cardiomyopathy in transgenic mice using comparative LC-MS analysis of thin fresh-frozen tissue sections.Journal of proteome research · 2012Article
- Cardiac and neuroprotection regulated by α(1)-adrenergic receptor subtypes.Journal of receptor and signal transduction research · 2011Review
- Attenuated hypertrophic response to pressure overload in a lamin A/C haploinsufficiency mouse.Journal of molecular and cellular cardiology · 2010Article
- Genetic analyses of the role of RCE1 in RAS membrane association and transformation.Methods in enzymology · 2008Review
- Hemojuvelin is essential for dietary iron sensing, and its mutation leads to severe iron overload.The Journal of clinical investigation · 2005Article
- Impact of treatment with melatonin on cerebral circulation in old rats.British journal of pharmacology · 2004Article
- Cardiomyopathy in Irx4-deficient mice is preceded by abnormal ventricular gene expression.Molecular and cellular biology · 2001Article
- Conditional expression of a Gi-coupled receptor causes ventricular conduction delay and a lethal cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Transgenic expression of replication-restricted enteroviral genomes in heart muscle induces defective excitation-contraction coupling and dilated cardiomyopathy.The Journal of clinical investigation · 1998Article
- Point mutations in human beta cardiac myosin heavy chain have differential effects on sarcomeric structure and assembly: an ATP binding site change disrupts both thick and thin filaments, whereas hypertrophic cardiomyopathy mutations display normal assembly.The Journal of cell biology · 1997Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
To overcome the genetic and interindividual variability frequently noted in complex phenotypes, we used echocardiographic selection to develop a substrain of myosin light chain (MLC)-Ras (RAS) transgenic mice with an enhanced ventricular hypertrophic phenotype. These echo-selected mice were then compared with wild-type (WT) animals and a pressure overload hypertrophy model (transverse aortic constriction; TAC). Echocardiography demonstrated increased wall thickness in RAS compared with the other groups. We developed novel miniaturized physiological technology to quantitatively identify in vivo intraventricular gradients; increased systolic Doppler velocity was seen in the left ventricle (LV) in 69% of RAS vs. none of WT or TAC. Intracavitary pressure gradients were present in 3 of 10 RAS vs. none of TAC or WT. Passive diastolic LV stiffness was not different among the three groups. Myofibrillar disarray was present in all RAS animals and was significantly more extensive (21.7% area fraction) than in TAC (1.5%) or WT (0.0%). RAS mice had selective induction of natriuretic peptide genes in the LV, a pattern distinct from that induced by pressure overload. Juvenile mortality was significantly increased in the offspring of echo-selected RAS parents. We conclude that adaptation of echocardiography to the mouse permits selection for cardiac phenotypes, and that selectively inbred MLC-Ras transgenic mice faithfully reproduce the molecular, physiological, and pathological features of human hypertrophic cardiomyopathy (HCM). Because previous studies support the concept that hypertrophy in human HCM is secondary to dysfunction created by sarcomeric protein mutations, the current studies suggest that Ras-dependent pathways might play a similar role in forms of human 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.