ReviewPflugers Archiv : European journal of physiology2005
Sarcomeric determinants of striated muscle relaxation kinetics.
Review in Pflugers Archiv : European journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 150 citations in OpenAlex.
- Piperine disrupts the OFF state of the resting thick filament of rat skeletal muscle, enhancing dynamic contractility in a fibre-type-dependent manner.The Journal of physiology · 2026Article
- The hypertrophic cardiomyopathy myosin variant G256E prolongs cardiac muscle relaxation via altered nucleotide handling.Communications chemistry · 2026Article
- Post Activation Potentiation Is Greater in Human Triceps Brachii Versus Triceps Surae Muscles.Muscle & nerve · 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
- Myosin-binding protein C slows cardiac myofibril relaxation kinetics.The Journal of physiology · 2025Article
- Theoretical treatment of tension transients in muscle following sudden changes in orthophosphate concentration: implications for energy transduction.Journal of muscle research and cell motility · 2025Article
- The elementary step that generates force and sinusoidal analysis in striated muscle fibers.Journal of muscle research and cell motility · 2025Review
- Dual-filament regulation of relaxation in mammalian fast skeletal muscle.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Postprandial cardiac hypertrophy is sustained by mechanics, epigenetic, and metabolic reprogramming in pythons.Proceedings of the National Academy of Sciences of the United States of America · 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
- A Laing distal myopathy-associated proline substitution in the β-myosin rod perturbs myosin cross-bridging activity.The Journal of clinical investigation · 2024Article
- Measuring the Contractile Kinetics of Isolated Myofibrils from Human-Induced Pluripotent Stem Cell Derived Cardiomyocyte (hiPSC-CM) Models of Cardiomyopathy.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Phosphate rebinding induces force reversal via slow backward cycling of cross-bridges.Frontiers in physiology · 2024Article
- Myosin-binding protein H-like regulates myosin-binding protein distribution and function in atrial cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Depressed myocardial cross-bridge cycling kinetics in a female guinea pig model of diastolic heart failure.The Journal of general physiology · 2023Article
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- Omecamtiv mecarbil augments cardiomyocyte contractile activity both at resting and systolic CaESC heart failure · 2023Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Ca2+ is the primary regulator of force generation by cross-bridges in striated muscle activation and relaxation. Relaxation is as necessary as contraction and, while the kinetics of Ca2+-induced force development have been investigated extensively, those of force relaxation have been both studied and understood less well. Knowledge of the molecular mechanisms underlying relaxation kinetics is of special importance for understanding diastolic function and dysfunction of the heart. A number of experimental models, from whole muscle organs and intact muscle fibres down to single myofibrils, have been used to explore the cascade of kinetic events leading to mechanical relaxation. By using isolated myofibrils and fast solution switching techniques we can distinguish the sarcomeric mechanisms of relaxation from those of myoplasmic Ca2+ removal. There is strong evidence that cross-bridge mechanics and kinetics are major determinants of the time course of striated muscle relaxation whilst thin filament inactivation kinetics and cooperative activation of thin filament by cycling, force-generating cross-bridges do not significantly limit the relaxation rate. Results in myofibrils can be explained well by a simple two-state model of the cross-bridge cycle in which the apparent rate of the force generating transition is modulated by fast, Ca2+-dependent equilibration between off- and on-states of actin. Inter-sarcomere dynamics during the final rapid phase of full force relaxation are responsible for deviations from this simple model.
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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.