ArticleJCI insight2019
Semaphorin 3E/PlexinD1 signaling is required for cardiac ventricular compaction.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Semaphorin 3E-Plexin-D1 Pathway Downstream of the Luteinizing Hormone Surge Regulates Ovulation, Granulosa Cell Luteinization, and Ovarian Angiogenesis in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Role of theGenes · 2025Article
- Bilateral Testicular Regression Syndrome and Optic Nerve Atrophy: Clinical Aspects of a Child with a <italic>SEMA3E</italic> Loss-of-Function Variant.Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation · 2025Article
- Plxnd1-mediated mechanosensing of blood flow controls the caliber of the Dorsal Aorta via the transcription factor Klf2.bioRxiv : the preprint server for biology · 2024Article
- Sox7-positive endothelial progenitors establish coronary arteries and govern ventricular compaction.EMBO reports · 2023Article
- Aberrant differentiation of second heart field mesoderm prefigures cellular defects in the outflow tract in response to loss of FGF8.Developmental biology · 2023Article
- Missense Mutation in Human CHD4 Causes Ventricular Noncompaction by Repressing ADAMTS1.Circulation research · 2023Article
- An X-linkedTranslational pediatrics · 2022Article
- Semaphorin3f as a cardiomyocyte derived regulator of heart chamber development.Cell communication and signaling : CCS · 2022Article
- Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish.eLife · 2022Article
- Left Ventricular Noncompaction Is Associated with Valvular Regurgitation and a Variety of Arrhythmias.Journal of cardiovascular development and disease · 2022Article
- Higher spatial resolution improves the interpretation of the extent of ventricular trabeculation.Journal of anatomy · 2022Article
- Endocardial-Myocardial Interactions During Early Cardiac Differentiation and Trabeculation.Frontiers in cardiovascular medicine · 2022Review
- Overlap phenotypes of the left ventricular noncompaction and hypertrophic cardiomyopathy with complex arrhythmias and heart failure induced by the novel truncated DSC2 mutation.Orphanet journal of rare diseases · 2021Article
- Endocardial/endothelial angiocrines regulate cardiomyocyte development and maturation and induce features of ventricular non-compaction.European heart journal · 2021Article
- Insights into the regulatory role of Plexin D1 signalling in cardiovascular development and diseases.Journal of cellular and molecular medicine · 2021Review
- Semaphorin3E-PlexinD1 signaling in coronary artery and lymphatic vessel development with clinical implications in myocardial recovery.iScience · 2021Article
- Mending a broken heart:Disease models & mechanisms · 2021Review
- Critical role of the BAF chromatin remodeling complex during murine neural crest development.PLoS genetics · 2021Article
- An Appreciation of Anatomy in the Molecular World.Journal of cardiovascular development and disease · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Left ventricular noncompaction (LVNC) is one of the most common forms of genetic cardiomyopathy characterized by excessive trabeculation and impaired myocardial compaction during fetal development. Patients with LVNC are at higher risk of developing left/right ventricular failure or both. Although the key regulators for cardiac chamber development are well studied, the role of semaphorin (Sema)/plexin signaling in this process remains poorly understood. In this article, we demonstrate that genetic deletion of Plxnd1, a class-3 Sema receptor in endothelial cells, leads to severe cardiac chamber defects. They were characterized by excessive trabeculation and noncompaction similar to patients with LVNC. Loss of Plxnd1 results in decreased expression of extracellular matrix proteolytic genes, leading to excessive deposition of cardiac jelly. We demonstrate that Plxnd1 deficiency is associated with an increase in Notch1 expression and its downstream target genes. In addition, inhibition of the Notch signaling pathway partially rescues the excessive trabeculation and noncompaction phenotype present in Plxnd1 mutants. Furthermore, we demonstrate that Semaphorin 3E (Sema3E), one of PlexinD1's known ligands, is expressed in the developing heart and is required for myocardial compaction. Collectively, our study uncovers what we believe to be a previously undescribed role of the Sema3E/PlexinD1 signaling pathway in myocardial trabeculation and the compaction process.
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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.