ArticleAnatomical record (Hoboken, N.J. : 2007)2019
Filamin-A as a Balance between Erk/Smad Activities During Cardiac Valve Development.
Article in Anatomical record (Hoboken, N.J. : 2007), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- The Role of Transforming Growth Factor-β Signaling in Myxomatous Mitral Valve Degeneration.Frontiers in cardiovascular medicine · 2022Pooled it
- Broadening horizons: new links between cilia and heart development and disease.Frontiers in cardiovascular medicine · 2026Review
- Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026Review
- Connective tissue disorders and cardiac arrhythmias: genetic pathways, mechanistic bridges, and clinical implications.Frontiers in cardiovascular medicine · 2026Review
- Article
- TGF-β phospho antibody array identifies altered SMAD2, PI3K/AKT/SMAD, and RAC signaling contribute to the pathogenesis of myxomatous mitral valve disease.Frontiers in veterinary science · 2023Article
- Interaction of LARP4 to filamin A mechanosensing domain regulates cell migrations.Frontiers in cell and developmental biology · 2023Article
- Intervertebral disc degeneration is rescued by TGFβ/BMP signaling modulation in an ex vivo filamin B mouse model.Bone research · 2022Article
- Mitral Valve Prolapse Induces Regionalized Myocardial Fibrosis.Journal of the American Heart Association · 2021Article
- Filamin A Regulates Cardiovascular Remodeling.International journal of molecular sciences · 2021Review
- PDGFRα: Expression and Function during Mitral Valve Morphogenesis.Journal of cardiovascular development and disease · 2021Article
- Mechanisms of heart valve development and disease.Development (Cambridge, England) · 2020Review
- Desert hedgehog-primary cilia cross talk shapes mitral valve tissue by organizing smooth muscle actin.Developmental biology · 2020Article
- Exploration of Oxygen-Induced Retinopathy Model to Discover New Therapeutic Drug Targets in Retinopathies.Frontiers in pharmacology · 2020Review
- The State of Cardiovascular Developmental Biology is Strong - Honoring Dr. Roger Markwald and his Seminal Contributions to the Field.Anatomical record (Hoboken, N.J. : 2007) · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Mitral valve prolapse (MVP) affects 2.4% of the population and has poorly understood etiology. Recent genetic studies have begun to unravel the complexities of MVP and through these efforts, mutations in the FLNA (Filamin-A) gene were identified as disease causing. Our in vivo and in vitro studies have validated these genetic findings and have revealed FLNA as a central regulator of valve morphogenesis. The mechanisms by which FLNA mutations result in myxomatous mitral valve disease are currently unknown, but may involve proteins previously associated with mutated regions of the FLNA protein, such as the small GTPase signaling protein, R-Ras. Herein, we report that Filamin-A is required for R-Ras expression and activation of the Ras-Mek-Erk pathway. Loss of the Ras/Erk pathway correlated with hyperactivation of pSmad2/3, increased extracellular matrix (ECM) production and enlarged mitral valves. Analyses of integrin receptors in the mitral valve revealed that Filamin-A was required for β1-integrin expression and provided a potential mechanism for impaired ECM compaction and valve enlargement. Our data support Filamin-A as a protein that regulates the balance between Erk and Smad activation and an inability of Filamin-A deficient valve interstitial cells to effectively remodel the increased ECM production through a β1-integrin mechanism. As a consequence, loss of Filamin-A function results in increased ECM production and generation of a myxomatous phenotype characterized by improperly compacted mitral valve tissue. Anat Rec, 302:117-124, 2019. © 2018 Wiley Periodicals, Inc.
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Registered trials
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