ArticleNature cardiovascular research2023
Titin governs myocardial passive stiffness with major support from microtubules and actin and the extracellular matrix.
Article in Nature cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Diastolic contributors in cardiomyocytes of a cardiometabolic HFpEF-like mouse model.The Journal of general physiology · 2026Article
- Integration of multiple perspectives to understand the left ventricular pressure-volume relationship.Communications medicine · 2026Review
- Sarcomere dynamic instability and stochastic heterogeneity drive robust cardiomyocyte contraction.eLife · 2026Article
- Adjunctive nebulization of Idursulfase to intravenous treatment enhances cardiac proteome adaptations in IDS-KO mice.bioRxiv : the preprint server for biology · 2026Article
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Variant Site-Specific Natural History of Titin-Induced Cardiomyopathy: An International Multicenter Registry.Circulation. Genomic and precision medicine · 2026Article
- Titin cleavage alters the myocardial elastic network and remodels the heart.Nature cardiovascular research · 2026Article
- Titin cleavage in living cardiomyocytes induces sarcomere disassembly but does not trigger cell proliferation.The Journal of biological chemistry · 2026Article
- Severe obesity in human HFpEF alters contractile protein function and organization.Science (New York, N.Y.) · 2026Article
- Selective titin cleavage disrupts cardiac mechanical homeostasis to drive heart failure and fibrosis.Nature cardiovascular research · 2026Article
- Right Heart Diastology, Where Are We Now?Circulation research · 2026Review
- Viscoelasticity of the Heart: An Overview of Viscoelastic Measurements at Different Scales.Annual review of biomedical engineering · 2026Review
- A primer on the methods of skeletal and cardiac muscle mechanics using permeabilized preparations.The Journal of general physiology · 2026Review
- Multi-omics Insight into Cardiac Myofibril Remodeling in Post-Prandial Burmese Pythons.bioRxiv : the preprint server for biology · 2026Article
- Mechanical Modeling of Cardiac Fibrosis With Explicit Spatial Representation of Cellular Structure and Collagen Alignment.Journal of biomechanical engineering · 2026Article
- Mending the Achilles heels of titin in cardiac and musculoskeletal disease.Biophysical reviews · 2026Review
- Fine-tuning striated muscle performance: conserved sarcomere-level mechanisms across insect and vertebrate systems.Frontiers in physiology · 2026Review
- Disulfidptosis in heart failure: an emerging mechanism awaiting exploration.Frontiers in cardiovascular medicine · 2026Review
- Machine Learning Reveals Novel Pediatric Heart Failure Phenotypes with Distinct Mortality and Hospitalization Outcomes.Diagnostics (Basel, Switzerland) · 2025Article
- Mechanically knocking out titin reveals protein tension loss as a trigger of muscle disease.Nature biomedical engineering · 2025Article
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Abstract
Myocardial passive stiffness is crucial for the heart's pump function and is determined by mechanical elements, including the extracellular matrix and cytoskeletal filaments; however, their individual contributions are controversially discussed and difficult to quantify. In this study, we targeted the cytoskeletal filaments in a mouse model, which enables the specific, acute and complete cleavage of the sarcomeric titin springs. We show in vitro that each cytoskeletal filament's stiffness contribution varies depending on whether the elastic or the viscous forces are considered and on strain level. Titin governs myocardial elastic forces, with the largest contribution provided at both low and high strain. Viscous force contributions are more uniformly distributed among the microtubules, titin and actin. The extracellular matrix contributes at high strain. The remaining forces after total target element disruption are likely derived from desmin filaments. Our findings answer longstanding questions about cardiac mechanical architecture and allow better targeting of passive myocardial stiffness in heart failure.
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