ArticlePediatric cardiology2018
Potential Common Pathogenic Pathways for the Left Ventricular Noncompaction Cardiomyopathy (LVNC).
Article in Pediatric cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed.
- Endocardial TIE2 orchestrates cardiac trabeculation via sequestering FOXO1 within the cytoplasm and stimulating versican cleavage.Development (Cambridge, England) · 2026Article
- Suppressive Genetic Interactions Between Haploinsufficient Mitochondrial Genes Encoded in the 22q11.2 Microdeletion Locus Define Brain and Cardiac Phenotypes.bioRxiv : the preprint server for biology · 2026Article
- Left Ventricular Noncompaction Cardiomyopathy in Children: A Focus on Genetic and Molecular Mechanisms.Reviews in cardiovascular medicine · 2025Review
- Deletion ofJournal of developmental biology · 2025Article
- Role of Col1a2 and Postn in left ventricular noncompaction cardiomyopathy.Journal of cardiothoracic surgery · 2025Article
- Establishment and functional studies of a model of cardiomyopathy with cardiomyocyte-specific conditional knockout of Arhgef18.Disease models & mechanisms · 2025Article
- Genetic and phenotypic architecture of human myocardial trabeculation.Nature cardiovascular research · 2024Article
- The mitochondrial citrate carrier SLC25A1 regulates metabolic reprogramming and morphogenesis in the developing heart.Communications biology · 2024Article
- Biventricular noncompaction induced heart failure in premature newborn.Radiology case reports · 2024Article
- Exploring Health Care Disparities in Genetic Testing and Research for Hereditary Cardiomyopathy: Current State and Future Perspectives.Global medical genetics · 2024Review
- Establishment and identification of cardiomyocyte arhGEF18 gene conditional knockout mice.Pediatric discovery · 2023Article
- A novel mutation in the TTN gene resulted in left ventricular noncompaction: a case report and literature review.BMC cardiovascular disorders · 2023Review
- Altered contractility, CaAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- Genetic Evaluation and Screening in Cardiomyopathies: Opportunities and Challenges for Personalized Medicine.Journal of personalized medicine · 2023Review
- Echocardiography phenotyping in murine genetic reference population of BXD strains reveals significant QTLs associated with cardiac function and morphology.Physiological genomics · 2023Article
- Left ventricular noncompaction: a disorder with genotypic and phenotypic heterogeneity-a narrative review.Cardiovascular diagnosis and therapy · 2022Review
- Article
- Imaging Features of Pediatric Left Ventricular Noncompaction Cardiomyopathy in Echocardiography and Cardiovascular Magnetic Resonance.Journal of cardiovascular development and disease · 2022Article
- PRDM16 Is a Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle.Circulation · 2022Article
- Left Ventricular Noncompaction Is Associated with Valvular Regurgitation and a Variety of Arrhythmias.Journal of cardiovascular development and disease · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Ventricular trabeculation and compaction are two essential morphogenetic events for generating a functionally competent ventricular wall. A significant reduction in trabeculation is usually associated with hypoplastic wall and ventricular compact zone deficiencies, which commonly leads to embryonic heart failure and early embryonic lethality. In contrast, the arrest of ventricular wall compaction (noncompaction) is believed to be causative to the left ventricular noncompaction (LVNC), a genetically heterogeneous disorder and the third most common cardiomyopathy among pediatric patients. After critically reviewing recent findings from genetically engineered mouse models, we suggest a model which proposes that defects in myofibrillogenesis and polarization in trabecular cardiomyocytes underly the common pathogenic mechanism for ventricular noncompaction.
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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.