ArticleThe Journal of general physiology2010
Model representation of the nonlinear step response in cardiac muscle.
Article in The Journal of general physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 47 citations in OpenAlex.
- Characterization of NEB pathogenic variants in patients reveals novel nemaline myopathy disease mechanisms and omecamtiv mecarbil force effects.Acta neuropathologica · 2024Article
- Proposing a Caputo-Land System for active tension. Capturing variable viscoelasticity.Heliyon · 2024Article
- Effect of the Novel Myotrope Danicamtiv on Cross-Bridge Behavior in Human Myocardium.Journal of the American Heart Association · 2023Article
- Shortening the thick filament by partial deletion of titin's C-zone alters cardiac function by reducing the operating sarcomere length range.Journal of molecular and cellular cardiology · 2022Article
- cMyBPC phosphorylation modulates the effect of omecamtiv mecarbil on myocardial force generation.The Journal of general physiology · 2021Article
- AAV9 gene transfer of cMyBPC N-terminal domains ameliorates cardiomyopathy in cMyBPC-deficient mice.JCI insight · 2020Article
- Strategies for targeting the cardiac sarcomere: avenues for novel drug discovery.Expert opinion on drug discovery · 2020Review
- Myocardial Contractility: Historical and Contemporary Considerations.Frontiers in physiology · 2020Article
- Developmental increase in β-MHC enhances sarcomere length-dependent activation in the myocardium.The Journal of general physiology · 2019Article
- The HCM-causing Y235S cMyBPC mutation accelerates contractile function by altering C1 domain structure.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Lost in translation: Interpreting cardiac muscle mechanics data in clinical practice.Archives of biochemistry and biophysics · 2019Review
- Sarcomere-based genetic enhancement of systolic cardiac function in a murine model of dilated cardiomyopathy.International journal of cardiology · 2018Article
- Impact of the Myosin Modulator Mavacamten on Force Generation and Cross-Bridge Behavior in a Murine Model of Hypercontractility.Journal of the American Heart Association · 2018Article
- Cardiomyopathy mutation (F88L) in troponin T abolishes length dependency of myofilament CaThe Journal of general physiology · 2018Article
- Omecamtiv Mecarbil Abolishes Length-Mediated Increase in Guinea Pig Cardiac Myofiber CaBiophysical journal · 2017Article
- Cardiac myosin binding protein-C SerScience advances · 2017Article
- Cardiomyopathy-related mutation (A30V) in mouse cardiac troponin T divergently alters the magnitude of stretch activation in α- and β-myosin heavy chain fibers.American journal of physiology. Heart and circulatory physiology · 2017Article
- L71F mutation in rat cardiac troponin T augments crossbridge recruitment and detachment dynamics against α-myosin heavy chain, but not against β-myosin heavy chain.Journal of muscle research and cell motility · 2016Article
- The effect of cardiomyopathy mutation (R97L) in mouse cardiac troponin T on the muscle length-mediated recruitment of crossbridges is modified divergently by α- and β-myosin heavy chain.Archives of biochemistry and biophysics · 2016Article
- Interplay between the effects of a Protein Kinase C phosphomimic (T204E) and a dilated cardiomyopathy mutation (K211Δ or R206W) in rat cardiac troponin T blunts the magnitude of muscle length-mediated crossbridge recruitment against the β-myosin heavy chain background.Journal of muscle research and cell motility · 2016Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
Motivated by the need for an analytical tool that can be used routinely to analyze data collected from isolated, detergent-skinned cardiac muscle fibers, we developed a mathematical model for representing the force response to step changes in muscle length (i.e., quick stretch and release). Our proposed model is reasonably simple, consisting of only five parameters representing: (1) the rate constant by which length change-induced distortion of elastic elements is dissipated; (2) the stiffness of the muscle fiber; (3) the amplitude of length-mediated recruitment of stiffness elements; (4) the rate constant by which this length-mediated recruitment takes place; and (5) the magnitude of the nonlinear interaction term by which distortion of elastic elements affects the number of recruited stiffness elements. Fitting this model to a family of force recordings representing responses to eight amplitudes of step length change (+/-2.0% baseline muscle length in 0.5% increments) enabled four things: (1) reproduction of all the identifiable features seen in a family of force responses to both positive and negative length changes; (2) close fitting of all records from the whole family of these responses with very little residual error; (3) estimation of all five model parameters with a great degree of certainty; and (4) importantly, ready discrimination between cardiac muscle fibers with different contractile regulatory proteins but showing only subtly different contractile function. We recommend this mathematical model as an analytic tool for routine use in studies of cardiac muscle fiber contractile function. Such model-based analysis gives novel insight to the contractile behavior of cardiac muscle fibers, and it is useful for characterizing the mechanistic effects that alterations of cardiac contractile proteins have on cardiac contractile function.
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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.