ReviewJournal of the Royal Society, Interface2011
Multi-scale computational models of familial hypertrophic cardiomyopathy: genotype to phenotype.
Review in Journal of the Royal Society, Interface, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- HeartSimSage: Attention-Enhanced Graph Neural Networks for Accelerating Cardiac Mechanics Modeling.Journal of computational physics · 2026Article
- The Evolution of Systems Biology and Systems Medicine: From Mechanistic Models to Uncertainty Quantification.Annual review of biomedical engineering · 2025Review
- Preclinical Models of Cardiac Disease: A Comprehensive Overview for Clinical Scientists.Cardiovascular engineering and technology · 2024Review
- Mechanisms of pathogenicity in the hypertrophic cardiomyopathy-associated TPM1 variant S215L.PNAS nexus · 2023Article
- Computational analysis of ventricular mechanics in hypertrophic cardiomyopathy patients.Scientific reports · 2023Article
- Strategies for targeting the cardiac sarcomere: avenues for novel drug discovery.Expert opinion on drug discovery · 2020Review
- Molecular Dynamics and Umbrella Sampling Simulations Elucidate Differences in Troponin C Isoform and Mutant Hydrophobic Patch Exposure.The journal of physical chemistry. B · 2018Article
- Blood flow patterns underlie developmental heart defects.American journal of physiology. Heart and circulatory physiology · 2017Article
- Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype.Frontiers in physiology · 2017Review
- Computational modeling of cardiac fibroblasts and fibrosis.Journal of molecular and cellular cardiology · 2016Review
- Modeling Pathologies of Diastolic and Systolic Heart Failure.Annals of biomedical engineering · 2016Article
- Towards causally cohesive genotype-phenotype modelling for characterization of the soft-tissue mechanics of the heart in normal and pathological geometries.Journal of the Royal Society, Interface · 2015Article
- Animal and in silico models for the study of sarcomeric cardiomyopathies.Cardiovascular research · 2015Review
- A new 4D trajectory-based approach unveils abnormal LV revolution dynamics in hypertrophic cardiomyopathy.PloS one · 2015Article
- Article
- Fibroblast-myocyte electrotonic coupling: does it occur in native cardiac tissue?Journal of molecular and cellular cardiology · 2014Review
- An integrative model of the cardiovascular system coupling heart cellular mechanics with arterial network hemodynamics.Journal of Korean medical science · 2013Article
- Combining wet and dry research: experience with model development for cardiac mechano-electric structure-function studies.Cardiovascular research · 2013Review
- Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α-tropomyosin.FEBS letters · 2012Article
- At the heart of computational modelling.The Journal of physiology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Familial hypertrophic cardiomyopathy (FHC) is an inherited disorder affecting roughly one in 500 people. Its hallmark is abnormal thickening of the ventricular wall, leading to serious complications that include heart failure and sudden cardiac death. Treatment is complicated by variation in the severity, symptoms and risks for sudden death within the patient population. Nearly all of the genetic lesions associated with FHC occur in genes encoding sarcomeric proteins, indicating that defects in cardiac muscle contraction underlie the condition. Detailed biophysical data are increasingly available for computational analyses that could be used to predict heart phenotypes based on genotype. These models must integrate the dynamic processes occurring in cardiac cells with properties of myocardial tissue, heart geometry and haemodynamic load in order to predict strain and stress in the ventricular walls and overall pump function. Recent advances have increased the biophysical detail in these models at the myofilament level, which will allow properties of FHC-linked mutant proteins to be accurately represented in simulations of whole heart function. The short-term impact of these models will be detailed descriptions of contractile dysfunction and altered myocardial strain patterns at the earliest stages of the disease-predictions that could be validated in genetically modified animals. Long term, these multi-scale models have the potential to improve clinical management of FHC through genotype-based risk stratification and personalized therapy.
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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.