ArticleBiophysical journal2013
Novel role for vinculin in ventricular myocyte mechanics and dysfunction.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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
23 citing papers in PubMed, 37 citations in OpenAlex.
- Connective tissue disorders and cardiac arrhythmias: genetic pathways, mechanistic bridges, and clinical implications.Frontiers in cardiovascular medicine · 2026Review
- Vinculin Y822 phosphorylation regulates adhesion remodeling during cardiomyocyte maturation.Journal of cell science · 2025Article
- Mechanics and disease of heart cells/cardiomyocytes explored through atomic force microscopy: present and future.Biophysical reviews · 2025Review
- From function to structure: how myofibrillogenesis influences the transverse-axial tubular system development and its peculiarities.Frontiers in physiology · 2025Review
- Myofilament dysfunction in diastolic heart failure.Heart failure reviews · 2024Review
- Subcellular Remodeling in Filamin C Deficient Mouse Hearts Impairs Myocyte Tension Development during Progression of Dilated Cardiomyopathy.International journal of molecular sciences · 2022Article
- An Implementation of Patient-Specific Biventricular Mechanics Simulations With a Deep Learning and Computational Pipeline.Frontiers in physiology · 2021Article
- Preserved cardiac function by vinculin enhances glucose oxidation and extends health- and life-span.APL bioengineering · 2018Article
- Review
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- Cardiac image modelling: Breadth and depth in heart disease.Medical image analysis · 2016Review
- Multi-scale Modeling of the Cardiovascular System: Disease Development, Progression, and Clinical Intervention.Annals of biomedical engineering · 2016Article
- Mechanical Regulation of Cardiac Aging in Model Systems.Circulation research · 2016Review
- Multiphysics and multiscale modelling, data-model fusion and integration of organ physiology in the clinic: ventricular cardiac mechanics.Interface focus · 2016Review
- Atomic Force Microscopy Protocol for Measurement of Membrane Plasticity and Extracellular Interactions in Single Neurons in Epilepsy.Frontiers in aging neuroscience · 2016Article
- Article
- The (dys)functional extracellular matrix.Biochimica et biophysica acta · 2015Review
- Vinculin network-mediated cytoskeletal remodeling regulates contractile function in the aging heart.Science translational medicine · 2015Article
- Mechanotransduction in cardiac hypertrophy and failure.Circulation research · 2015Review
- HACE1-dependent protein degradation provides cardiac protection in response to haemodynamic stress.Nature communications · 2014Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Vinculin (Vcl) plays a key structural role in ventricular myocytes that, when disrupted, can lead to contractile dysfunction and dilated cardiomyopathy. To investigate the role of Vcl in myocyte and myocardial function, cardiomyocyte-specific Vcl knockout mice (cVclKO) and littermate control wild-type mice were studied with transmission electron microscopy (TEM) and in vivo magnetic resonance imaging (MRI) tagging before the onset of global ventricular dysfunction. MRI revealed significantly decreased systolic strains transverse to the myofiber axis in vivo, but no changes along the muscle fibers or in fiber tension in papillary muscles from heterozygous global Vcl null mice. Myofilament lattice spacing from TEM was significantly greater in cVclKO versus wild-type hearts fixed in the unloaded state. AFM in Vcl heterozygous null mouse myocytes showed a significant decrease in membrane cortical stiffness. A multiscale computational model of ventricular mechanics incorporating cross-bridge geometry and lattice mechanics showed that increased transverse systolic stiffness due to increased lattice spacing may explain the systolic wall strains associated with Vcl deficiency, before the onset of ventricular dysfunction. Loss of cardiac myocyte Vcl may decrease systolic transverse strains in vivo by decreasing membrane cortical tension, which decreases transverse compression of the lattice thereby increasing interfilament spacing and stress transverse to the myofibers.
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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.