ArticleCurrent opinion in biomedical engineering2019
Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies.
Article in Current opinion in biomedical engineering, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 15 citations in OpenAlex.
- The Evolution of Systems Biology and Systems Medicine: From Mechanistic Models to Uncertainty Quantification.Annual review of biomedical engineering · 2025Review
- A homogenized constrained mixture model of cardiac growth and remodeling: analyzing mechanobiological stability and reversal.Biomechanics and modeling in mechanobiology · 2023Article
- Signaling network model of cardiomyocyte morphological changes in familial cardiomyopathy.Journal of molecular and cellular cardiology · 2023Article
- Characterization of Exercise-Induced Myocardium Growth Using Finite Element Modeling and Bayesian Optimization.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Myocardial hypertrophy is the result of sustained perturbations to the mechanical and/or neurohormonal homeostasis of cardiac cells and is driven by integrated, multiscale biophysical and biochemical processes that are currently not well defined. In this brief review, we highlight recent computational and experimental models of cardiac hypertrophy that span mechanisms from the molecular level to the tissue level. Specifically, we focus on: (i) molecular-level models of the structural dynamics of sarcomere proteins in hypertrophic hearts, (ii) cellular-level models of excitation-contraction coupling and mechanosensitive signaling in disease-state myocytes, and (iii) organ-level models of myocardial growth kinematics and predictors thereof. Finally, we discuss how spanning these scales and combining multiple experimental/computational models will provide new information about the processes governing hypertrophy and potential methods to prevent or reverse them.
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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.