ArticleCardiovascular research2017
Early sensitization of myofilaments to Ca2+ prevents genetically linked dilated cardiomyopathy in mice.
Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Risk Assessment and Personalized Treatment Options in Inherited Dilated Cardiomyopathies: A Narrative Review.Biomedicines · 2024Review
- Emerging Concepts of Mechanisms Controlling Cardiac Tension: Focus on Familial Dilated Cardiomyopathy (DCM) and Sarcomere-Directed Therapies.Biomedicines · 2024Review
- Nucleus Mechanosensing in Cardiomyocytes.International journal of molecular sciences · 2023Review
- A perspective on Notch signalling in progression and arrhythmogenesis in familial hypertrophic and dilated cardiomyopathies.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Comprehensive review on gene mutations contributing to dilated cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- The Hippo Signaling Pathway as a Drug Target in Familial Dilated Cardiomyopathy.International journal of drug discovery and pharmacology · 2022Article
- Association between High-Fat Diet during Pregnancy and Heart Weight of the Offspring: A Multivariate and Mediation Analysis.Nutrients · 2022Article
- Effects of Sarcomere Activators and Inhibitors Targeting Myosin Cross-Bridges on CaMolecular pharmacology · 2022Article
- Novel insights into sarcomere regulatory systems control of cardiac thin filament activation.The Journal of general physiology · 2021Article
- The intrinsically disordered C terminus of troponin T binds to troponin C to modulate myocardial force generation.The Journal of biological chemistry · 2019Article
- Sarcomeric mutations in cardiac diseases.Pflugers Archiv : European journal of physiology · 2019Article
- Tropomyosin pseudo-phosphorylation results in dilated cardiomyopathy.The Journal of biological chemistry · 2019Article
- Effects of cardiomyopathy-linked mutations K15N and R21H in tropomyosin on thin-filament regulation and pointed-end dynamics.Molecular biology of the cell · 2019Article
- Familial Dilated Cardiomyopathy Associated With a Novel Combination of Compound HeterozygousFrontiers in physiology · 2019Article
- Pathogenic troponin T mutants with opposing effects on myofilament CaArchives of biochemistry and biophysics · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundDilated cardiomoypathies (DCM) are a heterogeneous group of inherited and acquired diseases characterized by decreased contractility and enlargement of cardiac chambers and a major cause of morbidity and mortality. Mice with Glu54Lys mutation in α-tropomyosin (Tm54) demonstrate typical DCM phenotype with reduced myofilament Ca2+ sensitivity. We tested the hypothesis that early sensitization of the myofilaments to Ca2+ in DCM can prevent the DCM phenotype. METHODS AND
resultsTo sensitize Tm54 myofilaments, we used a genetic approach and crossbred Tm54 mice with mice expressing slow skeletal troponin I (ssTnI) that sensitizes myofilaments to Ca2+. Four groups of mice were used: non-transgenic (NTG), Tm54, ssTnI and Tm54/ssTnI (DTG). Systolic function was significantly reduced in the Tm54 mice compared to NTG, but restored in DTG mice. Tm54 mice also showed increased diastolic LV dimensions and HW/BW ratios, when compared to NTG, which were improved in the DTG group. β-myosin heavy chain expression was increased in the Tm54 animals compared to NTG and was partially restored in DTG group. Analysis by 2D-DIGE indicated a significant decrease in two phosphorylated spots of cardiac troponin I (cTnI) in the DTG animals compared to NTG and Tm54. Analysis by 2D-DIGE also indicated no significant changes in troponin T, regulatory light chain, myosin binding protein C and tropomyosin phosphorylation.
conclusionOur data indicate that decreased myofilament Ca2+ sensitivity is an essential element in the pathophysiology of thin filament linked DCM. Sensitization of myofilaments to Ca2+ in the early stage of DCM may be a useful therapeutic strategy in thin filament linked DCM.
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