ArticleJournal of cardiovascular development and disease2022
Significance of α-Myosin Heavy Chain (
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 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 32 citations in OpenAlex.
- Spatial multi-omic atlas profiles early organogenesis of a Carnegie stage 12 human embryo.Nature cell biology · 2026Article
- Diagnostic Yield of Exome Sequencing in Patients With Congenital Heart Disease From Southern Africa.Circulation. Genomic and precision medicine · 2026Article
- MYH6 in Congenital Heart Defects: A Genotype-Phenotype Characterization in a French Cohort.Pediatric cardiology · 2026Article
- Interpretable and scalable spatial gene set activity analysis with GESSO uncovers functional tissue architecture.bioRxiv : the preprint server for biology · 2026Article
- Elektra-Qki and Alien-Wt1 lncRNA-protein interaction controls myocardial ion channel expression and epicardial EMT during heart development in mice.Cellular and molecular life sciences : CMLS · 2026Article
- Bioactive factors in endometriosis peritoneal fluid remodel human cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2026Article
- Identification of the MYH6 c.804G>C Synonymous Variant Causing Exon Skipping in a Hypertrophic Cardiomyopathy Family.Molecular genetics & genomic medicine · 2026Article
- Landscape of copy number variants in Spanish people with dementia.NPJ genomic medicine · 2026Article
- Transcriptomic Insights into Micro- and Nanoplastic Toxicity in Zebrafish: A Narrative Review.Toxics · 2026Review
- ScalablebioRxiv : the preprint server for biology · 2026Article
- The Role of MYH6 Variants in atrial cardiomyopathy: insights from clinical observations and zebrafish models.NPJ genomic medicine · 2026Article
- Molecular insight into transcriptome profiling of aerobic exercise induced changes in aged skeletal muscle.npj aging · 2026Article
- Identification of novel and known variants inFrontiers in cardiovascular medicine · 2026Article
- Early Cytoskeletal Remodeling Drives Hypertrophic Cardiomyopathy Pathogenesis inJournal of cardiovascular development and disease · 2025Article
- Cardiac redox imbalance upon disruption of selenocysteine decomposition in mice.American journal of physiology. Heart and circulatory physiology · 2025Article
- Identifying Pathogenic Variants in Vietnamese Children with Functional Single Ventricle Based on Whole-Exome Sequencing.Diagnostics (Basel, Switzerland) · 2025Article
- New Genetic Loci Implicated in Cardiac Morphology and Function Using Three-Dimensional Population Phenotyping.Circulation. Genomic and precision medicine · 2025Article
- LncRNA HSCHARME is altered in human cardiomyopathies and promotes stem cell-derived cardiomyogenesis via splicing regulation.Nature communications · 2025Article
- Article
- Induced Pluripotent Stem Cells in Cardiomyopathy: Advancing Disease Modeling, Therapeutic Development, and Regenerative Therapy.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Hypoplastic left heart syndrome (HLHS) is a severe congenital heart disease (CHD) with complex genetic inheritance. HLHS segregates with other left ventricular outflow tract (LVOT) malformations in families, and can present as either an isolated phenotype or as a feature of a larger genetic disorder. The multifactorial etiology of HLHS makes it difficult to interpret the clinical significance of genetic variants. Specific genes have been implicated in HLHS, including rare, predicted damaging MYH6 variants that are present in >10% of HLHS patients, and which have been shown to be associated with decreased transplant-free survival in our previous studies. MYH6 (α-myosin heavy chain, α-MHC) variants have been reported in HLHS and numerous other CHDs, including LVOT malformations, and may provide a genetic link to these disorders. In this paper, we outline the MYH6 variants that have been identified, discuss how bioinformatic and functional studies can inform clinical decision making, and highlight the importance of genetic testing in HLHS.
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What OpenQuestion holds
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.