ArticleJournal of molecular and cellular cardiology2011
Titin based viscosity in ventricular physiology: an integrative investigation of PEVK-actin interactions.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Diastolic contributors in cardiomyocytes of a cardiometabolic HFpEF-like mouse model.The Journal of general physiology · 2026Article
- Effects of chemical myosin II cross-bridge inhibitors on eccentric force production in skinned muscle fibres.Experimental physiology · 2026Article
- Viscoelasticity of the Heart: An Overview of Viscoelastic Measurements at Different Scales.Annual review of biomedical engineering · 2026Review
- Chronic and acute mediators of passive viscoelasticity in human skeletal muscle fibres.Experimental physiology · 2025Article
- Theoretical analysis of power-law stress relaxation and calcium-dependent passive mechanics in cardiac muscle.The Journal of physiology · 2025Article
- Titin's Intrinsically Disordered PEVK Domain Modulates Actin Polymerization.International journal of molecular sciences · 2025Article
- Glycerol storage increases passive stiffness of muscle fibers through effects on titin extensibility.The Journal of general physiology · 2025Article
- The L348P point mutation in cardiac myosin binding protein-C alters transient responses to stretch, slows cardiac relaxation, and is embryonic lethal in homozygous CRISPR gene-edited mice.Journal of molecular and cellular cardiology · 2025Article
- 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
- hsa-miR-548v controls the viscoelastic properties of human cardiomyocytes and improves their relaxation rates.JCI insight · 2024Article
- Increased Chamber Resting Tone Is a Key Determinant of Left Ventricular Diastolic Dysfunction.Circulation. Heart failure · 2023Article
- Strain-dependent stress relaxation behavior of healthy right ventricular free wall.Acta biomaterialia · 2022Article
- The Super-Relaxed State and Length Dependent Activation in Porcine Myocardium.Circulation research · 2021Article
- Power Amplification Increases With Contraction Velocity During Stretch-Shortening Cycles of Skinned Muscle Fibers.Frontiers in physiology · 2021Article
- Need for Speed: The Importance of Physiological Strain Rates in Determining Myocardial Stiffness.Frontiers in physiology · 2021Article
- The Effects of Mechanical Preload on Transmural Differences in Mechano-Calcium-Electric Feedback in Single Cardiomyocytes: Experiments and Mathematical Models.Frontiers in physiology · 2020Article
- Extensive eccentric contractions in intact cardiac trabeculae: revealing compelling differences in contractile behaviour compared to skeletal muscles.Proceedings. Biological sciences · 2019Article
- The link between exercise and titin passive stiffness.Experimental physiology · 2017Review
- Cell- and molecular-level mechanisms contributing to diastolic dysfunction in HFpEF.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Review
- Deleting titin's I-band/A-band junction reveals critical roles for titin in biomechanical sensing and cardiac function.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Viscosity is proposed to modulate diastolic function, but only limited understanding of the source(s) of viscosity exists. In vitro experiments have shown that the proline-glutamic acid-valine-lysine (PEVK) rich element of titin interacts with actin, causing a viscous force in the sarcomere. It is unknown whether this mechanism contributes to viscosity in vivo. We tested the hypothesis that PEVK-actin interaction causes cardiac viscosity and is important in vivo via an integrative physiological study on a unique PEVK knockout (KO) model. Both skinned cardiomyocytes and papillary muscle fibers were isolated from wildtype (WT) and PEVK KO mice and passive viscosity was examined using stretch-hold-release and sinusoidal analysis. Viscosity was reduced by ~60% in KO myocytes and ~50% in muscle fibers at room temperature. The PEVK-actin interaction was not modulated by temperature or diastolic calcium, but was increased by lattice compression. Stretch-hold and sinusoidal frequency protocols on intact isolated mouse hearts showed a smaller, 30-40% reduction in viscosity, possibly due to actomyosin interactions, and showed that microtubules did not contribute to viscosity. Transmitral Doppler echocardiography similarly revealed a 40% decrease in LV chamber viscosity in the PEVK KO in vivo. This integrative study is the first to quantify the influence of a specific molecular (PEVK-actin) viscosity in vivo and shows that PEVK-actin interactions are an important physiological source of viscosity.
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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.