ReviewMedicina (Kaunas, Lithuania)2023
Hypertrophic Cardiomyopathy: Genetic Foundations, Outcomes, Interconnections, and Their Modifiers.
Review in Medicina (Kaunas, Lithuania), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- A large-scale single-nucleus resource reveals a cardiomyocyte-like fibroblast and stage-specific remodeling across cardiomyopathies.BMC medicine · 2026Article
- Genotype-Phenotype Discordance in Cardiomyopathies: Pathophysiology, Clinical Expression, and Therapeutic Considerations.Health science reports · 2026Article
- Article
- Are clinical trajectories in obstructive hypertrophic cardiomyopathy mutation-specific? A systematic review and meta-analysis ofFrontiers in cardiovascular medicine · 2026Review
- Tobacco use disorder is associated with increased risk of cardiomyopathy in a population-based study from Taiwan.Scientific reports · 2025Article
- Hypertrophic Cardiomyopathy: Current Perspectives.Reviews in cardiovascular medicine · 2025Review
- The MYH7 c.2770G > A (p.Glu924Lys) mutation exhibits phenotypic heterogeneity in hypertrophic cardiomyopathy (HCM) and restrictive cardiomyopathy (RCM): a case report.BMC cardiovascular disorders · 2025Article
- Review
- Mass Spectrometric ITEM-FOUR Analysis Reveals Coding Single-Nucleotide Polymorphisms in Human Cardiac Troponin T That Evade Detection by Sandwich ELISAs Which Use Monoclonal Antibodies M7 and M11.7 from the Elecsys Troponin TInternational journal of molecular sciences · 2025Article
- Exploring the c.406 C > T variant in TNNI3 gene: pathogenic insights into restrictive cardiomyopathy.BMC medical genomics · 2025Article
- KLF9 aggravates the cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy through the lncRNA UCA1/p27 axis.International journal of experimental pathology · 2025Article
- Patterns of Increased Cardiomyocyte Ploidy in Myocardial Hypertrophy of Various Origins.Bulletin of experimental biology and medicine · 2025Article
- HCM-Echo-VAR-Ensemble: Deep Ensemble Fusion to Detect Hypertrophic Cardiomyopathy in Echocardiograms.IEEE open journal of engineering in medicine and biology · 2025Article
- Integrated Multi-omics Analysis of Hub Genes and miRNA Interactions in Hypertrophic Cardiomyopathy.Current genomics · 2025Article
- Cardiomyopathies: The Role of Non-Coding RNAs.Non-coding RNA · 2024Review
- Deciphering metabolomics and lipidomics landscape in zebrafish hypertrophic cardiomyopathy model.Scientific reports · 2024Article
- Genetic Mutations and Mitochondrial Redox Signaling as Modulating Factors in Hypertrophic Cardiomyopathy: A Scoping Review.International journal of molecular sciences · 2024Article
- Transcriptomics data integration and analysis to uncover hallmark genes in hypertrophic cardiomyopathy.American journal of translational research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hypertrophic cardiomyopathy (HCM) is the most prevalent heritable cardiomyopathy. HCM is considered to be caused by mutations in cardiac sarcomeric protein genes. Recent research suggests that the genetic foundation of HCM is much more complex than originally postulated. The clinical presentations of HCM are very variable. Some mutation carriers remain asymptomatic, while others develop severe HCM, terminal heart failure, or sudden cardiac death. Heterogeneity regarding both genetic mutations and the clinical course of HCM hinders the establishment of universal genotype-phenotype correlations. However, some trends have been identified. The presence of a mutation in some genes encoding sarcomeric proteins is associated with earlier HCM onset, more severe left ventricular hypertrophy, and worse clinical outcomes. There is a diversity in the mechanisms implicated in the pathogenesis of HCM. They may be classified into groups, but they are interrelated. The lack of known supplementary elements that control the progression of HCM indicates that molecular mechanisms that exist between genotype and clinical presentations may be crucial. Secondary molecular changes in pathways implicated in HCM pathogenesis, post-translational protein modifications, and epigenetic factors affect HCM phenotypes. Cardiac loading conditions, exercise, hypertension, diet, alcohol consumption, microbial infection, obstructive sleep apnea, obesity, and environmental factors are non-molecular aspects that change the HCM phenotype. Many mechanisms are implicated in the course of HCM. They are mostly interconnected and contribute to some extent to final outcomes.
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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.