ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Impaired relaxation is the main manifestation in transgenic mice expressing a restrictive cardiomyopathy mutation, R193H, in cardiac TnI.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- Troponin: biology, molecular mechanisms, and multidimensional clinical applications.Molecular biomedicine · 2026Review
- Echocardiographic Assessment of Cardiac Function in Mouse Models of Heart Disease.International journal of molecular sciences · 2025Review
- Troponin I - a comprehensive review of its function, structure, evolution, and role in muscle diseases.Animal cells and systems · 2025Review
- Exploring contractile protein mechanisms and target medications for cardiomyopathic patients with diastolic dysfunction.Pediatric discovery · 2024Review
- Angiotensin Receptor-Neprilysin Inhibition (Sacubitril/Valsartan) Reduces Structural Arterial Stiffness in Middle-Aged Mice.Journal of the American Heart Association · 2024Article
- Gene correction and overexpression of TNNI3 improve impaired relaxation in engineered heart tissue model of pediatric restrictive cardiomyopathy.Development, growth & differentiation · 2024Article
- Sarcomeric gene variants among Indians with hypertrophic cardiomyopathy: A scoping review.The Indian journal of medical research · 2023Article
- Intact Transition Epitope Mapping-Force Differences between Original and Unusual Residues (ITEM-FOUR).Biomolecules · 2023Article
- Cardiac Sarcomere Signaling in Health and Disease.International journal of molecular sciences · 2022Review
- Complex roads from genotype to phenotype in dilated cardiomyopathy: scientific update from the Working Group of Myocardial Function of the European Society of Cardiology.Cardiovascular research · 2018Review
- Role of Whole-exome Sequencing in Phenotype Classification and Clinical Treatment of Pediatric Restrictive Cardiomyopathy.Chinese medical journal · 2017Article
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Clinical and Mechanistic Insights Into the Genetics of Cardiomyopathy.Journal of the American College of Cardiology · 2016Review
- Green tea extract catechin improves internal cardiac muscle relaxation in RCM mice.Journal of biomedical science · 2016Article
- TNNI1, TNNI2 and TNNI3: Evolution, regulation, and protein structure-function relationships.Gene · 2016Review
- Restrictive Cardiomyopathy Caused by Troponin Mutations: Application of Disease Animal Models in Translational Studies.Frontiers in physiology · 2016Review
- Human Engineered Heart Muscles Engraft and Survive Long Term in a Rodent Myocardial Infarction Model.Circulation research · 2015Article
- N-Acetyl Cysteine improves the diabetic cardiac function: possible role of fibrosis inhibition.BMC cardiovascular disorders · 2015Article
- Cell biology of sarcomeric protein engineering: disease modeling and therapeutic potential.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
- Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review.Frontiers in physiology · 2014Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Transgenic mice were generated to express a restrictive cardiomyopathy (RCM) human cardiac troponin I (cTnI) R192H mutation in the heart (cTnI(193His) mice). The objective of this study was to assess cardiac function during the development of diastolic dysfunction and to gain insight into the pathophysiological impact of the RCM cTnI mutation. Cardiac function and pathophysiological changes were monitored in cTnI193His mice and wild-type littermates for a period of 12 mo. It progressed gradually from abnormal relaxation to diastolic dysfunction characterized with high-resolution echocardiography by a reversed E-to-A ratio, increased deceleration time, and prolonged isovolumetric relaxation time. At the age of 12 mo, cardiac output in cTnI(193His) mice was significantly declined, and some transgenic mice showed congestive heart failure. The negative impact of cTnI193His on ventricular contraction and relaxation was further demonstrated in isolated mouse working heart preparations. The main morphological change in cTnI193His myocytes was shortened cell length. Dobutamine stimulation increased heart rate in cTnI193His mice but did not improve CO. The cTnI193His mice had a phenotype similar to that in human RCM patients carrying the cTnI mutation characterized morphologically by enlarged atria and restricted ventricles and functionally by diastolic dysfunction and diastolic heart failure. The results demonstrate a critical role of the COOH-terminal domain of cTnI in the diastolic function of cardiac muscle.
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