ArticleJournal of cardiovascular development and disease2022
DCHS1, Lix1L, and the Septin Cytoskeleton: Molecular and Developmental Etiology of Mitral Valve Prolapse.
Article in Journal of cardiovascular development and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026Review
- Dynamic Expression and Functional Implications of the Cell Polarity Gene, Dchs1, During Cardiac Development.Cells · 2025Article
- Neuronal hyperactivity in neurons derived from individuals with gray matter heterotopia.Nature communications · 2025Article
- Patient-derived induced pluripotent stem cells with aWorld journal of stem cells · 2024Article
- Differential Development of the Chordae Tendineae and Anterior Leaflet of the Bovine Mitral Valve.Journal of cardiovascular development and disease · 2024Article
- Ovol1/2 loss-induced epidermal defects elicit skin immune activation and alter global metabolism.EMBO reports · 2023Article
- Septins as membrane influencers: direct play or in association with other cytoskeleton partners.Frontiers in cell and developmental biology · 2023Review
- Non-syndromal mitral valve prolapse (MVP): a common entity, but not commonly associated withJournal of thoracic disease · 2022Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Mitral valve prolapse (MVP) is a common cardiac valve disease that often progresses to serious secondary complications requiring surgery. MVP manifests as extracellular matrix disorganization and biomechanically incompetent tissues in the adult setting. However, MVP has recently been shown to have a developmental basis, as multiple causal genes expressed during embryonic development have been identified. Disease phenotypes have been observed in mouse models with human MVP mutations as early as birth. This study focuses on the developmental function of DCHS1, one of the first genes to be shown as causal in multiple families with non-syndromic MVP. By using various biochemical techniques as well as mouse and cell culture models, we demonstrate a unique link between DCHS1-based cell adhesions and the septin-actin cytoskeleton through interactions with cytoplasmic protein Lix1-Like (LIX1L). This DCHS1-LIX1L-SEPT9 axis interacts with and promotes filamentous actin organization to direct cell-ECM alignment and valve tissue shape.
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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 Socratic graph.