ArticleJournal of molecular biology2009
Functional effects of a restrictive-cardiomyopathy-linked cardiac troponin I mutation (R145W) in transgenic mice.
Article in Journal of molecular biology, 2009. 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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Who cites it
32 citing papers in PubMed.
- Human Variant in the Cardiac Troponin I Switch Domain Causes Diastolic Dysfunction in a Novel Mouse Model.Journal of the American Heart Association · 2025Article
- Troponin I - a comprehensive review of its function, structure, evolution, and role in muscle diseases.Animal cells and systems · 2025Review
- Impaired Relaxation in Induced Pluripotent Stem Cell-Derived Cardiomyocytes with PathogenicJournal of the American Heart Association · 2024Article
- Exploring contractile protein mechanisms and target medications for cardiomyopathic patients with diastolic dysfunction.Pediatric discovery · 2024Review
- Assessing Cardiac Contractility From Single Molecules to Whole Hearts.JACC. Basic to translational science · 2024Review
- Gene correction and overexpression of TNNI3 improve impaired relaxation in engineered heart tissue model of pediatric restrictive cardiomyopathy.Development, growth & differentiation · 2024Article
- Engineered cardiac tissue model of restrictive cardiomyopathy for drug discovery.Cell reports. Medicine · 2023Article
- Genome Editing and Pathological Cardiac Hypertrophy.Advances in experimental medicine and biology · 2023Article
- Cardiac Sarcomere Signaling in Health and Disease.International journal of molecular sciences · 2022Review
- Genotype-Phenotype Associations with Restrictive Cardiomyopathy Induced by Pathogenic Genetic Mutations.Reviews in cardiovascular medicine · 2022Review
- Article
- Cardiac troponin I R193H mutant interacts with HDAC1 to repress phosphodiesterase 4D expression in cardiomyocytes.Genes & diseases · 2021Article
- Potential impacts of the cardiac troponin I mobile domain on myofilament activation and relaxation.Journal of molecular and cellular cardiology · 2021Article
- Mutation location of HCM-causing troponin T mutations defines the degree of myofilament dysfunction in human cardiomyocytes.Journal of molecular and cellular cardiology · 2021Article
- Where Does Inflammation Fit?Current cardiology reports · 2017Review
- Proteasome dysfunction in cardiomyopathies.The Journal of physiology · 2017Review
- Acute Optogenetic Modulation of Cardiac Twitch Dynamics Explored Through Modeling.Journal of biomechanical engineering · 2016Article
- Restrictive Cardiomyopathy Troponin I R145W Mutation Does Not Perturb Myofilament Length-dependent Activation in Human Cardiac Sarcomeres.The Journal of biological chemistry · 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
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The human cardiac troponin I (hcTnI) mutation R145W has been associated with restrictive cardiomyopathy. In this study, simultaneous measurements of ATPase activity and force in skinned papillary fibers from hcTnI R145W transgenic mice (Tg-R145W) were explored. Tg-R145W fibers showed an approximately 13-16% increase in maximal Ca(2+)-activated force and ATPase activity compared to hcTnI wild-type transgenic mice. The force-generating cross-bridge turnover rate (g) and the energy cost (ATPase/force) were the same in all groups of fibers. Also, the Tg-R145W fibers showed a large increase in the Ca(2+) sensitivity of both force development and ATPase. In intact fibers, the mutation caused prolonged force and intracellular [Ca(2+)] transients and increased time to peak force. Analysis of force and Ca(2+) transients showed that there was a 40% increase in peak force in Tg-R145W muscles, which was likely due to the increased Ca(2+) transient duration. The above cited results suggest that: (1) there would be an increase in resistance to ventricular filling during diastole resulting from the prolonged force and Ca(2+) transients that would result in a decrease in ventricular filling (diastolic dysfunction); and (2) there would be a large (approximately 53%) increase in force during systole, which may help to partly compensate for diastolic dysfunction. These functional results help to explain the mechanisms by which these mutations give rise to a restrictive phenotype.
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