ArticleThe American journal of pathology2004
Heterozygous inactivation of the vinculin gene predisposes to stress-induced cardiomyopathy.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 115 citations in OpenAlex.
- Cardiomyocyte-Specific Smad7 Protects the Pressure-Overloaded Heart, Inhibiting the Transforming Growth Factor-β Receptor 1/Smad2/3 Cascade.Journal of the American Heart Association · 2026Article
- Vinculin mediates a dynamic signal flow underlying cardiac outflow tract development as revealed by single-cell and spatial transcriptomic analysis.Journal of advanced research · 2026Article
- The vinculin-β-catenin axis promotes bone formation and repair: an essential prerequisite for the anti-osteoporotic efficacy of sclerostin-neutralizing antibody.Science China. Life sciences · 2026Article
- Vinculin influences essential processes in enteric nervous system development and Hirschsprung disease pathogenesis.The Journal of clinical investigation · 2026Article
- Vinculin haploinsufficiency impairs integrin-mediated costamere remodeling on stiffer microenvironments.Journal of molecular and cellular cardiology · 2025Article
- Unveiling the Spectrum of Minor Genes in Cardiomyopathies: A Narrative Review.International journal of molecular sciences · 2024Review
- Focal Adhesion's Role in Cardiomyocytes Function: From Cardiomyogenesis to Mechanotransduction.Cells · 2024Review
- Molecular basis and cellular functions of vinculin-actin directional catch bonding.Nature communications · 2023Article
- Heart Failure with Recovered Ejection Fraction in Patients with Vinculin Loss-of-function Variants.Journal of cardiovascular translational research · 2023Article
- Cardiotoxicity as a Possible Side Effect of Statins.Reviews in cardiovascular medicine · 2023Review
- Review of Recent Laboratory and Experimental Data on Cardiotoxicity of Statins.Journal of cardiovascular development and disease · 2022Review
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- Myocardial Hypertrophy and Compensatory Increase in Systolic Function in a Mouse Model of Oxidative Stress.International journal of molecular sciences · 2021Article
- The Cryogenic Electron Microscopy Structure of the Cell Adhesion Regulator Metavinculin Reveals an Isoform-Specific Kinked Helix in Its Cytoskeleton Binding Domain.International journal of molecular sciences · 2021Article
- Metavinculin modulates force transduction in cell adhesion sites.Nature communications · 2020Article
- An assessment of the role of vinculin loss of function variants in inherited cardiomyopathy.Human mutation · 2020Article
- Collagen, stiffness, and adhesion: the evolutionary basis of vertebrate mechanobiology.Molecular biology of the cell · 2020Review
- ZO-1 Regulates Intercalated Disc Composition and Atrioventricular Node Conduction.Circulation research · 2020Article
- Distinct Binding Modes of Vinculin Isoforms Underlie Their Functional Differences.Structure (London, England : 1993) · 2019Article
- Mechanical stability of αT-catenin and its activation by force for vinculin binding.Molecular biology of the cell · 2019Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Vinculin and its muscle splice variant metavinculin link focal adhesions and cell-to-cell contact sites to the actin cytoskeleton. We hypothesized that normal expression of vinculin isoforms would be essential for integrity of cardiomyocytes and preservation of normal cardiac function. We studied heterozygous vinculin knockout mice (Vin+/-) that develop and breed normally. The Vin+/- mice displayed: 1) a 58% reduction of vinculin and a 63% reduction of metavinculin protein levels versus wild-type littermates; 2) normal basal cardiac function and histology but abnormal electrocardiograms, intercalated disks, and ICD-related protein distribution; 3) increased mortality following acute hemodynamic stress imposed by transverse aortic constriction (TAC); 4) cardiac dysfunction by 6 weeks post-TAC; and 5) misalignment of alpha-actinin containing Z-lines and abnormal myocardial ultrastructure despite preserved cardiac function. Decreased expression of vinculin/metavinculin leads to abnormal myocyte structure without baseline physiological evidence of cardiac dysfunction. These structural changes predispose to stress-induced cardiomyopathy.
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Registered trials
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