ArticleJournal of muscle research and cell motility2003
Gigantic variety: expression patterns of titin isoforms in striated muscles and consequences for myofibrillar passive stiffness.
Article in Journal of muscle research and cell motility, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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98 citing papers in PubMed, 193 citations in OpenAlex.
- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
- Transcript-aware rare genetic variant association analyses of cardiopulmonary traits in participants from the All of Us Research Program.Nature communications · 2026Article
- 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
- Mending the Achilles heels of titin in cardiac and musculoskeletal disease.Biophysical reviews · 2026Review
- TTN variants in pediatric cardiomyopathy: a retrospective cohort study.Frontiers in genetics · 2026Article
- Understanding inherited cardiomyopathies: clinical aspects and genetic determinants.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2025Article
- Rbm24-mediated post-transcriptional regulation of skeletal and cardiac muscle development, function and regeneration.Journal of muscle research and cell motility · 2025Review
- An overview of insights and updates on TTN mutations in cardiomyopathies.Frontiers in pharmacology · 2025Review
- Alternative Splicing in the Heart: The Therapeutic Potential of Regulating the Regulators.International journal of molecular sciences · 2024Review
- Impact of lengthening velocity on the generation of eccentric force by slow-twitch muscle fibers in long stretches.Pflugers Archiv : European journal of physiology · 2024Article
- RNA-Binding Proteins in Cardiomyopathies.Journal of cardiovascular development and disease · 2024Review
- Exploring TTN variants as genetic insights into cardiomyopathy pathogenesis and potential emerging clues to molecular mechanisms in cardiomyopathies.Scientific reports · 2024Review
- Expression of Smyd1b_tv1 by Alternative Splicing in Cardiac Muscle is Critical for Sarcomere Organization in Cardiomyocytes and Heart Function.Molecular and cellular biology · 2024Article
- Heart Failure with Preserved Ejection Fraction: a Pharmacotherapeutic Update.Cardiovascular drugs and therapy · 2023Review
- Characterizing residual and passive force enhancements in cardiac myofibrils.Biophysical journal · 2023Article
- Titin activates myosin filaments in skeletal muscle by switching from an extensible spring to a mechanical rectifier.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Gaining new understanding of sarcomere length non-uniformities in skeletal muscles.Frontiers in physiology · 2023Article
- Contributions of Titin and Collagen to Passive Stress in Muscles fromInternational journal of molecular sciences · 2022Article
- Protein Quality Control at the Sarcomere: Titin Protection and Turnover and Implications for Disease Development.Frontiers in physiology · 2022Review
38 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The giant muscle protein titin has become a focus of research interests in the field of muscle mechanics due to its importance for passive muscle stiffness. Here we summarize research activities leading to current understanding of titin's mechanical role in the sarcomere. We then show how low-porosity polyacrylamide-gel electrophoresis, optimised for resolving megadalton proteins, can identify differences in titin-isoform expression in the hearts of 10 different vertebrate species and in several skeletal muscles of the rabbit. A large variety of titin-expression patterns is apparent, which is analysed in terms of its effect on the passive tension of isolated myofibrils obtained from selected muscle types. We show and discuss evidence indicating that vertebrate striated muscle cells are capable of adjusting their passive stiffness in the following ways: (1) Cardiomyocytes co-express long (N2BA) and short (N2B) titin isoform in the same half-sarcomeres and vary the N2BA:N2B ratio to adjust stiffness. Hearts from different mammalian species vary widely in their N2BA:N2B ratio; right ventricles show higher ratios than left ventricles. There is also a significant gradient of N2BA:N2B ratio in a given heart, from basal to apical; transmural ratio differences are less distinct. (2) Skeletal muscles can express longer or shorter I-band-titin (N2A-isoform) to achieve lower or higher titin-derived stiffness, respectively. (3) Some skeletal muscles co-express longer (N2A(L)) and shorter (N2A(S)) titin isoforms, also at the single-fibre level (e.g., rabbit psoas); variations in overall N2A(L):N2A(S) ratio may add to the fine-tuning of titin-based stiffness in the whole muscle. Whereas it is established that titin, together with extracellular collagen, determines the passive tension at physiological sarcomere lengths in cardiac muscle, it remains to be seen to which degree titin and/or extracellular structures are important for the physiological passive-tension generation of whole skeletal muscle.
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