ArticleCurrent cardiology reviews2009
Titin and troponin: central players in the frank-starling mechanism of the heart.
Article in Current cardiology reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 49 citations in OpenAlex.
- Temperature dependence of activation of thick and thin filaments in skeletal and cardiac muscles.Journal of muscle research and cell motility · 2026Review
- Myosin-actin crossbridge independent sarcomere length induced CaJournal of molecular and cellular cardiology · 2025Article
- CaJournal of molecular and cellular cardiology · 2025Article
- Regulation of myocardial contraction as revealed by intracellular CaThe journal of physiological sciences : JPS · 2024Review
- Cardiac efficiency and Starling's Law of the Heart.The Journal of physiology · 2022Article
- Cardiac CT perfusion and FFRCardiovascular diagnosis and therapy · 2020Review
- Nanoscopic changes in the lattice structure of striated muscle sarcomeres involved in the mechanism of spontaneous oscillatory contraction (SPOC).Scientific reports · 2020Article
- Mechano-calcium and mechano-electric feedbacks in the human cardiomyocyte analyzed in a mathematical model.The journal of physiological sciences : JPS · 2020Article
- Nitric Oxide and Mechano-Electrical Transduction in Cardiomyocytes.Frontiers in physiology · 2020Review
- Thermal Activation of Thin Filaments in Striated Muscle.Frontiers in physiology · 2020Review
- Microscopic heat pulses activate cardiac thin filaments.The Journal of general physiology · 2019Article
- Sarcomere length-dependent effects on CaThe Journal of general physiology · 2019Article
- Role of the C-terminus mobile domain of cardiac troponin I in the regulation of thin filament activation in skinned papillary muscle strips.Archives of biochemistry and biophysics · 2018Article
- Pre-mRNA mis-splicing of sarcomeric genes in heart failure.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Cardiomyocyte Hypocontractility and Reduced Myofibril Density in End-Stage Pediatric Cardiomyopathy.Frontiers in physiology · 2017Article
- A Spatially Detailed Model of Isometric Contraction Based on Competitive Binding of Troponin I Explains Cooperative Interactions between Tropomyosin and Crossbridges.PLoS computational biology · 2015Article
- In situ time-resolved FRET reveals effects of sarcomere length on cardiac thin-filament activation.Biophysical journal · 2014Article
- Cardiac thin filament regulation and the Frank-Starling mechanism.The journal of physiological sciences : JPS · 2014Review
- Maladaptive modifications in myofilament proteins and triggers in the progression to heart failure and sudden death.Pflugers Archiv : European journal of physiology · 2014Review
- Structural basis for the in situ Ca(2+) sensitization of cardiac troponin C by positive feedback from force-generating myosin cross-bridges.Archives of biochemistry and biophysics · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The basis of the Frank-Starling mechanism of the heart is the intrinsic ability of cardiac muscle to produce greater active force in response to stretch, a phenomenon known as length-dependent activation. A feedback mechanism transmitted from cross-bridge formation to troponin C to enhance Ca(2+) binding has long been proposed to account for length-dependent activation. However, recent advances in muscle physiology research technologies have enabled the identification of other factors involved in length-dependent activation. The striated muscle sarcomere contains a third filament system composed of the giant elastic protein titin, which is responsible for most passive stiffness in the physiological sarcomere length range. Recent studies have revealed a significant coupling of active and passive forces in cardiac muscle, where titin-based passive force promotes cross-bridge recruitment, resulting in greater active force production in response to stretch. More currently, the focus has been placed on the troponin-based "on-off" switching of the thin filament state in the regulation of length-dependent activation. In this review, we discuss how myocardial length-dependent activation is coordinately regulated by sarcomere proteins.
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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.