ReviewNature reviews. Cardiology2011
Mechanisms of disease: hypertrophic cardiomyopathy.
Review in Nature reviews. Cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.
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
121 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
- Metabolomic biomarkers and metabolic remodelling in genetically characterised hypertrophic cardiomyopathy: a systematic review.Metabolomics : Official journal of the Metabolomic Society · 2026Pooled it
- Development of a Multi-Organ Microphysiological (MPS) Model to Study Age-Related Comorbidities.Advanced biology · 2026Article
- AMPKγ2 Regulates Cardiac Hypertrophy and Arrhythmias via Interacting With Myosin.Circulation research · 2026Article
- Generation of two induced pluripotent stem cell lines from hypertrophic cardiomyopathy patients carrying MYBPC3 mutations.Stem cell research · 2026Article
- Precision Cardiogenomics in Athletes.International journal of molecular sciences · 2026Review
- Editorial: Case Reports in general cardiovascular medicine: 2024.Frontiers in cardiovascular medicine · 2026Article
- Lower left ventricular ejection time in MYBPC3 variant carriers with overt or subclinical hypertrophic cardiomyopathy.ESC heart failure · 2025Article
- Tubulin tyrosine ligase variant perturbs microtubule tyrosination, causing hypertrophy in patient-specific and CRISPR gene-edited iPSC-cardiomyocytes.JCI insight · 2025Article
- Review
- The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review.Non-coding RNA research · 2025Review
- Increased Plasma Pyruvate Kinase M2 (PK-M2) in Heart Failure: A Novel Biomarker Related to Cardiac Function and its Clinical Implications.Journal of the American Heart Association · 2025Article
- An overview of insights and updates on TTN mutations in cardiomyopathies.Frontiers in pharmacology · 2025Review
- scGO: interpretable deep neural network for cell status annotation and disease diagnosis.Briefings in bioinformatics · 2024Article
- A Machine Learning Approach to Gene Expression in Hypertrophic Cardiomyopathy.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Substrate mechanics unveil early structural and functional pathology in iPSC micro-tissue models of hypertrophic cardiomyopathy.iScience · 2024Article
- The abnormalities of free fatty acid metabolism in patients with hypertrophic cardiomyopathy, a single-center retrospective observational study.BMC cardiovascular disorders · 2024Observational
- Arrhythmias and Hypertrophic Cardiomyopathy: Unravelling the Connection.Current cardiology reviews · 2024Review
- Missense mutations in the central domains of cardiac myosin binding protein-C and their potential contribution to hypertrophic cardiomyopathy.The Journal of biological chemistry · 2024Article
- Rationale and design of a randomised trial of trientine in patients with hypertrophic cardiomyopathy.Heart (British Cardiac Society) · 2023Article
- Identification of circRNA-miRNA-mRNA regulatory network and its role in cardiac hypertrophy.PloS one · 2023Article
61 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM) is the most-common monogenically inherited form of heart disease, characterized by thickening of the left ventricular wall, contractile dysfunction, and potentially fatal arrhythmias. HCM is also the most-common cause of sudden cardiac death in individuals younger than 35 years of age. Much progress has been made in the elucidation of the genetic basis of HCM, resulting in the identification of more than 900 individual mutations in over 20 genes. Interestingly, most of these genes encode sarcomeric proteins, such as myosin-7 (also known as cardiac muscle β-myosin heavy chain; MYH7), cardiac myosin-binding protein C (MYBPC3), and cardiac muscle troponin T (TNNT2). However, the molecular events that ultimately lead to the clinical phenotype of HCM are still unclear. We discuss several potential pathways, which include altered calcium cycling and sarcomeric calcium sensitivity, increased fibrosis, disturbed biomechanical stress sensing, and impaired cardiac energy homeostasis. An improved understanding of the pathological mechanisms involved will result in greater specificity and success of therapies for patients with HCM.
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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.