ArticleCardiovascular research2008
Differential interactions of thin filament proteins in two cardiac troponin T mouse models of hypertrophic and dilated cardiomyopathies.
Article in Cardiovascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Obstructive hypertrophic cardiomyopathy: from genetic insights to a multimodal therapeutic approach with mavacamten, aficamten, and beyond.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- A Revised Perspective on the Evolution of Troponin I and Troponin T Gene Families in Vertebrates.Genome biology and evolution · 2023Article
- Modeling Nonischemic Genetic Cardiomyopathies Using Induced Pluripotent Stem Cells.Current cardiology reports · 2022Review
- Molecular Genetic Basis of Hypertrophic Cardiomyopathy.Circulation research · 2021Article
- Cardiac Overexpression of XIN Prevents Dilated Cardiomyopathy Caused byFrontiers in cell and developmental biology · 2021Article
- Translating emerging molecular genetic insights into clinical practice in inherited cardiomyopathies.Journal of molecular medicine (Berlin, Germany) · 2018Review
- The genetics of hypertrophic cardiomyopathy.Global cardiology science & practice · 2018Review
- Suppression of Activated FOXO Transcription Factors in the Heart Prolongs Survival in a Mouse Model of Laminopathies.Circulation research · 2018Article
- Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy.Circulation research · 2017Review
- Natural genetic variation of the cardiac transcriptome in non-diseased donors and patients with dilated cardiomyopathy.Genome biology · 2017Article
- Genetics and Genomics of Single-Gene Cardiovascular Diseases: Common Hereditary Cardiomyopathies as Prototypes of Single-Gene Disorders.Journal of the American College of Cardiology · 2016Review
- In Utero Caffeine Exposure Induces Transgenerational Effects on the Adult Heart.Scientific reports · 2016Article
- Gene-Targeted Mice with the Human Troponin T R141W Mutation Develop Dilated Cardiomyopathy with Calcium Desensitization.PloS one · 2016Article
- Exome Sequencing Identifies Pathogenic and Modifier Mutations in a Child With Sporadic Dilated Cardiomyopathy.Journal of the American Heart Association · 2015Article
- Generation of a tamoxifen inducible Tnnt2MerCreMer knock-in mouse model for cardiac studies.Genesis (New York, N.Y. : 2000) · 2015Article
- The functional effect of dilated cardiomyopathy mutation (R144W) in mouse cardiac troponin T is differently affected by α- and β-myosin heavy chain isoforms.American journal of physiology. Heart and circulatory physiology · 2015Article
- Research priorities in sarcomeric cardiomyopathies.Cardiovascular research · 2015Review
- Oxidative Stress in Dilated Cardiomyopathy Caused by MYBPC3 Mutation.Oxidative medicine and cellular longevity · 2015Article
- Clinical Potentials of Cardiomyocytes Derived from Patient-Specific Induced Pluripotent Stem Cells.Journal of clinical medicine · 2014Review
- Human induced pluripotent stem cell-derived cardiomyocytes as an in vitro model for coxsackievirus B3-induced myocarditis and antiviral drug screening platform.Circulation research · 2014Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
aimMutations in a sarcomeric protein can cause hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM), the opposite ends of a spectrum of phenotypic responses of the heart to mutations. We posit the contracting phenotypes could result from differential effects of the mutant proteins on interactions among the sarcomeric proteins. To test the hypothesis, we generated transgenic mice expressing either cardiac troponin T (cTnT)-Q92 or cTnT-W141, known to cause HCM and DCM, respectively, in the heart. METHODS AND
resultsWe phenotyped the mice by echocardiography, histology and immunoblotting, and real-time polymerase chain reaction. We detected interactions between the sarcomeric proteins by co-immunoprecipitation and determined Ca2+ sensitivity of myofibrillar protein ATPase activity by Carter assay. The cTnT-W141 mice exhibited dilated hearts and decreased systolic function. In contrast, the cTnT-Q92 mice showed smaller ventricles and enhanced systolic function. Levels of cardiac troponin I, cardiac alpha-actin, alpha-tropomyosin, and cardiac troponin C co-immunoprecipitated with anti-cTnT antibodies were higher in the cTnT-W141 than in the cTnT-Q92 mice, as were levels of alpha-tropomyosin co-immunoprecipitated with an anti-cardiac alpha-actin antibody. In contrast, levels of cardiac troponin I co-immunoprecipitated with an anti-cardiac alpha-actin antibody were higher in the cTnT-Q92 mice. Ca2+ sensitivity of myofibrillar ATPase activity was increased in HCM but decreased in DCM mice compared with non-transgenic mice.
conclusionDifferential interactions among the sarcomeric proteins containing cTnT-Q92 or cTnT-W141 are responsible for the contrasting phenotypes of HCM or DCM, respectively.
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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.