ReviewArchives of biochemistry and biophysics2019
How myofilament strain and strain rate lead the dance of the cardiac cycle.
Review in Archives of biochemistry and biophysics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- A Drosophila cardiac myosin increases jump muscle stretch activation and shortening deactivation.Biophysical journal · 2025Article
- Molecular regulation of stretch activation.American journal of physiology. Cell physiology · 2022Article
- Reduced preload increases Mechanical Control (strain-rate dependence) of Relaxation by modifying myosin kinetics.Archives of biochemistry and biophysics · 2021Article
- Move quickly to detach: Strain rate-dependent myosin detachment and cardiac relaxation.The Journal of general physiology · 2020Article
- Current and Future Directions of Myofilament Regulation.Archives of biochemistry and biophysics · 2019Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Movement of the myocardium can modify organ-level cardiac function and its molecular (crossbridge) mechanisms. This motion, which is defined by myocardial strain and strain rate (muscle shortening, lengthening, and the speed of these movements), occurs throughout the cardiac cycle, including during isovolumic periods. This review highlights how the left ventricular myocardium moves throughout the cardiac cycle, how muscle mechanics experiments provide insight into the regulation of forces used to move blood in and out of the left ventricle, and its impact on (and regulation by) crossbridge and sarcomere kinetics. We specifically highlight how muscle mechanics experiments explain how myocardial relaxation is accelerated by lengthening (strain rate) during late systole and isovolumic relaxation, a lengthening which has been measured in human hearts. Advancing and refining both in vivo measurement and ex vivo protocols with physiologic strain and strain rates could reveal important insights into molecular (crossbridge) kinetics. These advances could provide an improvement in both diagnosis and precise treatment of cardiac dysfunction.
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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.