ArticleAmerican journal of physiology. Heart and circulatory physiology2015
A dilated cardiomyopathy mutation blunts adrenergic response and induces contractile dysfunction under chronic angiotensin II stress.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Dobutamine Stress Echocardiography for Left Ventricular Reverse Remodeling in Idiopathic Dilated Cardiomyopathy.International journal of heart failure · 2025Article
- 5,7-Dimethoxychroman-3-yl 4-methoxybenzoate Has a Unique Effect upon the Modulation of Mutant Cardiac Muscle Thin Filament Function and Dynamics due to Phosphorylation of Troponin I.ACS pharmacology & translational science · 2025Article
- Focus on cardiac troponin complex: From gene expression to cardiomyopathy.Genes & diseases · 2024Review
- Nutraceuticals silybin B, resveratrol, and epigallocatechin-3 gallate-bind to cardiac muscle troponin to restore the loss of lusitropy caused by cardiomyopathy mutationsFrontiers in physiology · 2024Article
- Modulation of Structure and Dynamics of Cardiac Troponin by Phosphorylation and Mutations Revealed by Molecular Dynamics Simulations.The journal of physical chemistry. B · 2023Article
- Recent studies of the molecular mechanism of lusitropy due to phosphorylation of cardiac troponin I by protein kinase A.Journal of muscle research and cell motility · 2023Review
- Suppression of lusitropy as a disease mechanism in cardiomyopathies.Frontiers in cardiovascular medicine · 2022Review
- Small Molecules acting on Myofilaments as Treatments for Heart and Skeletal Muscle Diseases.International journal of molecular sciences · 2020Review
- Troponin structure and function: a view of recent progress.Journal of muscle research and cell motility · 2020Review
- Approaches to High-Throughput Analysis of Cardiomyocyte Contractility.Frontiers in physiology · 2020Article
- Increased myocyte calcium sensitivity in end-stage pediatric dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Article
- Phenotyping an adult zebrafish lamp2 cardiomyopathy model identifies mTOR inhibition as a candidate therapy.Journal of molecular and cellular cardiology · 2019Article
- Small molecule studies: the fourth wave of muscle research.Journal of muscle research and cell motility · 2019Article
- Phenotyping cardiomyopathy in adult zebrafish.Progress in biophysics and molecular biology · 2018Review
- Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes.Scientific reports · 2017Article
- Mutations in troponin T associated with Hypertrophic Cardiomyopathy increase Ca(2+)-sensitivity and suppress the modulation of Ca(2+)-sensitivity by troponin I phosphorylation.Archives of biochemistry and biophysics · 2016Article
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4 authors at 1 institution in 1 country.
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Abstract
We investigated cardiac contractility in the ACTC E361G transgenic mouse model of dilated cardiomyopathy (DCM). No differences in cardiac dimensions or systolic function were observed in young mice, whereas young adult mice exhibited only mild diastolic abnormalities. Dobutamine had an inotropic and lusitropic effect on the mouse heart. In papillary muscle at 37°C, dobutamine increased relaxation rates [∼50% increase of peak rate of force decline normalized to force (dF/dtmin/F), 25% reduction of time to 90% relaxation (t90) in nontransgenic (NTG) mice], but in the ACTC E361G mouse, dF/dtmin/F was increased 20-30%, and t90 was only reduced 10% at 10 Hz. Pressure-volume measurements showed increases in maximum rate of pressure decline and decreases in time constant of left ventricular pressure decay in the ACTC E361G mouse that were 25-30% of the changes in the NTG mouse, consistent with blunting of the lusitropic response. The inotropic effect of dobutamine was also blunted in ACTC E361G mice, and the dobutamine-stimulated increase in cardiac output (CO) was reduced from 2,100 to 900 μl/min. Mice were treated with high doses of ANG II for 4 wk. The chronic stress treatment evoked systolic dysfunction in ACTC E361G mice but not in NTG. There was a significant reduction in rates of pressure increase and decrease, as well as reduced end-systolic pressure and increased volume. Ejection fraction and CO were reduced in the ACTC E361G mouse, indicating DCM. In vitro DCM-causing mutations uncouple the relationship between Ca(2+) sensitivity and troponin I phosphorylation. We conclude that this leads to the observed, reduced response to β1 agonists and reduced cardiac reserve that predisposes the heart to DCM under conditions of chronic stress.
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