ArticleJournal of molecular and cellular cardiology2011
Calcium binding kinetics of troponin C strongly modulate cooperative activation and tension kinetics in cardiac muscle.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 80 citations in OpenAlex.
- Evolutionary and physics-guided modulation of CaJournal of molecular modeling · 2026Article
- Hypercontractile phenotype at rest in chronic coronary syndromes predicts impaired functional reserve and increased mortality.ESC heart failure · 2026Article
- The hypertrophic cardiomyopathy myosin variant G256E prolongs cardiac muscle relaxation via altered nucleotide handling.Communications chemistry · 2026Article
- Multiscale computational modeling of the cardiopulmonary consequences of postnatal hyperoxia with implications for preterm-born children.Biomechanics and modeling in mechanobiology · 2026Article
- Molecular mechanisms of altered contraction with the β-myosin R403Q mutation in porcine ventricular muscle and a human stem cell-derived cardiomyocyte model.Journal of molecular and cellular cardiology · 2025Article
- Preventing hypocontractility-induced fibroblast expansion alleviates dilated cardiomyopathy.Science (New York, N.Y.) · 2025Article
- Multiscale Computational Modeling of the Cardiopulmonary Consequences of Postnatal Hyperoxia with Implications for Preterm Born Children.bioRxiv : the preprint server for biology · 2025Article
- Review
- Modeling the effects of thin filament near-neighbor cooperative interactions in mammalian myocardium.The Journal of general physiology · 2025Article
- Mechanisms of a novel regulatory light chain-dependent cardiac myosin inhibitor.The Journal of general physiology · 2024Article
- MYBPC3-c.772G>A mutation results in haploinsufficiency and altered myosin cycling kinetics in a patient induced stem cell derived cardiomyocyte model of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology · 2024Article
- Incomplete-penetrant hypertrophic cardiomyopathyProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Troponin I Tyrosine Phosphorylation Beneficially Accelerates Diastolic Function.Circulation research · 2024Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Danicamtiv Increases Myosin Recruitment and Alters Cross-Bridge Cycling in Cardiac Muscle.Circulation research · 2023Article
- Mouse Models of Cardiomyopathies Caused by Mutations in Troponin C.International journal of molecular sciences · 2023Review
- Differences in Effects of Length-Dependent Regulation of Force and CaInternational journal of molecular sciences · 2023Article
- Using Multiscale Simulations as a Tool to Interpret Equatorial X-ray Fiber Diffraction Patterns from Skeletal Muscle.International journal of molecular sciences · 2023Article
- Machine learning meets Monte Carlo methods for models of muscle's molecular machinery to classify mutations.The Journal of general physiology · 2023Article
- Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Tension development and relaxation in cardiac muscle are regulated at the thin filament via Ca(2+) binding to cardiac troponin C (cTnC) and strong cross-bridge binding. However, the influence of cTnC Ca(2+)-binding properties on these processes in the organized structure of cardiac sarcomeres is not well-understood and likely differs from skeletal muscle. To study this we generated single amino acid variants of cTnC with altered Ca(2+) dissociation rates (k(off)), as measured in whole troponin (cTn) complex by stopped-flow spectroscopy (I61Q cTn>WT cTn>L48Q cTn), and exchanged them into cardiac myofibrils and demembranated trabeculae. In myofibrils at saturating Ca(2+), L48Q cTnC did not affect maximum tension (T(max)), thin filament activation (k(ACT)) and tension development (k(TR)) rates, or the rates of relaxation, but increased duration of slow phase relaxation. In contrast, I61Q cTnC reduced T(max), k(ACT) and k(TR) by 40-65% with little change in relaxation. Interestingly, k(ACT) was less than k(TR) with I61Q cTnC, and this difference increased with addition of inorganic phosphate, suggesting that reduced cTnC Ca(2+)-affinity can limit thin filament activation kinetics. Trabeculae exchanged with I61Q cTn had reduced T(max), Ca(2+) sensitivity of tension (pCa(50)), and slope (n(H)) of tension-pCa, while L48Q cTn increased pCa(50) and reduced n(H). Increased cross-bridge cycling with 2-deoxy-ATP increased pCa(50) with WT or L48Q cTn, but not I61Q cTn. We discuss the implications of these results for understanding the role of cTn Ca(2+)-binding properties on the magnitude and rate of tension development and relaxation in cardiac muscle.
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