ArticleCirculation2005
Transgenic rabbit model for human troponin I-based hypertrophic cardiomyopathy.
Article in Circulation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 74 citations in OpenAlex.
- Experimental Models of Hypertrophic Cardiomyopathy: A Systematic Review.JACC. Basic to translational science · 2025Review
- Molecular Pathways and Animal Models of Cardiomyopathies.Advances in experimental medicine and biology · 2024Article
- ESC working group on cardiac cellular electrophysiology position paper: relevance, opportunities, and limitations of experimental models for cardiac electrophysiology research.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2021Review
- Genetic basis and molecular biology of cardiac arrhythmias in cardiomyopathies.Cardiovascular research · 2020Review
- Hypertrophic cardiomyopathy R403Q mutation in rabbit β-myosin reduces contractile function at the molecular and myofibrillar levels.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Upregulation of Myocardial and Vascular Phosphodiesterase 9A in A Model of Atherosclerotic Cardiovascular Disease.International journal of molecular sciences · 2018Article
- Quantification of Beat-To-Beat Variability of Action Potential Durations in Langendorff-Perfused Mouse Hearts.Frontiers in physiology · 2018Article
- A One Health Approach to Hypertrophic Cardiomyopathy.The Yale journal of biology and medicine · 2017Review
- In Vivo Analysis of Troponin C Knock-In (A8V) Mice: Evidence that TNNC1 Is a Hypertrophic Cardiomyopathy Susceptibility Gene.Circulation. Cardiovascular genetics · 2015Article
- Ultrastructural changes, increased oxidative stress, inflammation, and altered cardiac hypertrophic gene expressions in heart tissues of rats exposed to incense smoke.Environmental science and pollution research international · 2015Article
- Animal and in silico models for the study of sarcomeric cardiomyopathies.Cardiovascular research · 2015Review
- Small and large animal models in cardiac contraction research: advantages and disadvantages.Pharmacology & therapeutics · 2014Review
- Passive ventricular remodeling in cardiac disease: focus on heterogeneity.Frontiers in physiology · 2014Review
- Inherited cardiomyopathies caused by troponin mutations.Journal of geriatric cardiology : JGC · 2013Article
- A quantitative comparison of regional myocardial motion in mice, rabbits and humans using in-vivo phase contrast CMR.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2012Article
- Diastolic dysfunction and thin filament dysregulation resulting from excitation-contraction uncoupling in a mouse model of restrictive cardiomyopathy.Journal of molecular and cellular cardiology · 2012Article
- Lost in transgenesis: a user's guide for genetically manipulating the mouse in cardiac research.Circulation research · 2012Review
- On the emerging role of rabbit as human disease model and the instrumental role of novel transgenic tools.Transgenic research · 2012Review
- Increased myofilament Ca2+-sensitivity and arrhythmia susceptibility.Journal of molecular and cellular cardiology · 2010Review
- Role of animal models in HCM research.Journal of cardiovascular translational research · 2009Review
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14 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTransgenic and gene-targeted models have focused on the mouse. Fundamental differences between the mouse and human exist in Ca2+ handling during contraction/relaxation and in alterations in Ca2+ flux during heart failure, with the rabbit more accurately reflecting the human system. METHODS AND
resultsCardiac troponin I (cTnI) mutations can cause familial hypertrophic cardiomyopathy. An inhibitory domain mutation, arginine146-->glycine (cTnI(146Gly)), was modeled with the use of transgenic expression in the rabbit ventricle. cTnI(146Gly) levels >40% of total cTnI were perinatally lethal, whereas replacement levels of 15% to 25% were well tolerated. cTnI(146Gly) expression led to a leftward shift in the force-pCa2+ curves with cardiomyocyte disarray, fibrosis, and altered connexin43 organization. In isolated cTnI(146Gly) myocytes, twitch relaxation amplitudes were smaller than in normal cells, but [Ca]i transients and sarcoplasmic reticulum Ca2+ load were not different. Detrended fluctuation analysis of the QT(max) intervals was used to evaluate the cardiac repolarization phase and showed a significantly higher scaling exponent in the transgenic animals.
conclusionsExpression of modest amounts of cTnI(146Gly) led to subtle defects without severely affecting cardiac function. Aberrant connexin organization, subtle morphological deficits, and an altered fractal pattern of the repolarization phase of transgenic rabbits, in the absence of entropy or other ECG abnormalities, may indicate an early developing pathology before the onset of more obvious repolarization abnormalities or major alterations in cardiac mechanics.
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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.