ReviewMolecular biology of the cell2016
Biology of the cardiac myocyte in heart disease.
Review in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed.
- Genetic determinants of heart failure susceptibility and response in the collaborative cross mouse population.Genetics · 2026Article
- Plant Terpenoids in Cardioprotection: An Overview of Their Therapeutic Potential.Current issues in molecular biology · 2026Review
- Versatile hiPSC Models and Bioengineering Platforms for Investigation of Atrial Fibrosis and Fibrillation.Cells · 2026Review
- Molecular insights in HIV-associated cardiac dysfunction.Communications medicine · 2025Article
- Exploring in vivo and in vitro models for heart failure with biomarker insights: a review.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- Transcriptomic Approaches to Cardiomyocyte-Biomaterial Interactions: A Review.ACS biomaterials science & engineering · 2024Review
- Review
- Tailoring transfection for cardiomyocyte cell lines: balancing efficiency and toxicity in lipid versus polymer-based transfection methods in H9c2 and HL-1 cells.American journal of physiology. Heart and circulatory physiology · 2024Article
- Optimization of H9c2 differentiation leads to calcium-active and striated cardiac cells without addition of retinoic acid.Frontiers in cell and developmental biology · 2024Article
- Nanomedicine And Nanotheranostics: Special Focus on Imaging of Anticancer Drugs Induced Cardiac Toxicity.Nanotheranostics · 2024Review
- Single-Cell Analysis of Contractile Forces in iPSC-Derived Cardiomyocytes: Paving the Way for Precision Medicine in Cardiovascular Disease.International journal of molecular sciences · 2023Article
- Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart-Part I: Experimental Injury Models to Study Cardiac Regeneration.Journal of cardiovascular development and disease · 2023Review
- Review
- Three tyrosine kinase inhibitors cause cardiotoxicity by inducing endoplasmic reticulum stress and inflammation in cardiomyocytes.BMC medicine · 2023Article
- FK506-Binding Protein like (FKBPL) Has an Important Role in Heart Failure with Preserved Ejection Fraction Pathogenesis with Potential Diagnostic Utility.Biomolecules · 2023Article
- An efficient human stem cells derived cardiotoxicity testing platform for testing oncotherapeutic analogues of quercetin and cinnamic acid.Scientific reports · 2022Article
- Merits of hiPSC-Derived Cardiomyocytes for In Vitro Research and Testing Drug Toxicity.Biomedicines · 2022Article
- Myocardial infarction from a tissue engineering and regenerative medicine point of view: A comprehensive review on models and treatments.Biophysics reviews · 2022Review
- Upregulation of Phospholipase C Gene Expression Due to Norepinephrine-Induced Hypertrophic Response.Cells · 2022Review
- Review
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.
Funding
Abstract
Cardiac hypertrophy is a major risk factor for heart failure, and it has been shown that this increase in size occurs at the level of the cardiac myocyte. Cardiac myocyte model systems have been developed to study this process. Here we focus on cell culture tools, including primary cells, immortalized cell lines, human stem cells, and their morphological and molecular responses to pathological stimuli. For each cell type, we discuss commonly used methods for inducing hypertrophy, markers of pathological hypertrophy, advantages for each model, and disadvantages to using a particular cell type over other in vitro model systems. Where applicable, we discuss how each system is used to model human disease and how these models may be applicable to current drug therapeutic strategies. Finally, we discuss the increasing use of biomaterials to mimic healthy and diseased hearts and how these matrices can contribute to in vitro model systems of cardiac cell biology.
Indexed as
Identifiers
What Socratic 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 Socratic graph.