ArticleCirculation research2019
Identifying the Transcriptome Signatures of Calcium Channel Blockers in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.
Article in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Pooled it
- New approach methodologies: drug screening platform to identify antifibrotic compounds.Nature protocols · 2026Review
- Metabolic crisis and TRPM4 activation cause QT prolongation in TANGO2 deficiency disorder.Cardiovascular research · 2026Article
- Matured hiPSC-derived cardiomyocytes possess dematuration plasticity.Journal of molecular and cellular cardiology plus · 2025Article
- Temporal Patterns of Holter-Detected Arrhythmias in Hypertrophic Cardiomyopathy Patients Treated with Mavacamten.Biomedicines · 2025Article
- Pharmacogenomics and its Role in Cardiovascular Diseases: A Narrative Literature Review.Current cardiology reviews · 2025Review
- Informing Hazard Identification and Risk Characterization of Environmental Chemicals by Combining Transcriptomic and Functional Data from Human-Induced Pluripotent Stem-Cell-Derived Cardiomyocytes.Chemical research in toxicology · 2024Article
- Application of Calcium Kinetics Characterization in Cardiac Disease Modeling and Drug Discovery.Biomolecules · 2024Article
- Transcriptomic Approaches to Cardiomyocyte-Biomaterial Interactions: A Review.ACS biomaterials science & engineering · 2024Review
- Do calcium channel blockers applied to cardiomyocytes cause increased channel expression resulting in reduced efficacy?NPJ systems biology and applications · 2024Article
- iPSC-cardiomyocytes in the preclinical prediction of candidate pharmaceutical toxicity.Frontiers in pharmacology · 2024Review
- Quantification of Cardiomyocyte Contraction In Vitro and Drug Screening by MyocytoBeats.Journal of cardiovascular translational research · 2023Article
- Systems analysis of de novo mutations in congenital heart diseases identified a protein network in the hypoplastic left heart syndrome.Cell systems · 2022Article
- Technical Applications of Microelectrode Array and Patch Clamp Recordings on Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes.Journal of visualized experiments : JoVE · 2022Article
- Review
- Activation of PDGFRA signaling contributes to filamin C-related arrhythmogenic cardiomyopathy.Science advances · 2022Article
- Application of hiPSC as a Drug TesterFrontiers in genetics · 2022Review
- Human Engineered Heart Tissue Models for Disease Modeling and Drug Discovery.Frontiers in cell and developmental biology · 2022Review
- Sarcomere function activates a p53-dependent DNA damage response that promotes polyploidization and limits in vivo cell engraftment.Cell reports · 2021Article
- Genetic Cardiomyopathies: The Lesson Learned from hiPSCs.Journal of clinical medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
rationaleCalcium channel blockers (CCBs) are an important class of drugs in managing cardiovascular diseases. Patients usually rely on these medications for the remainder of their lives after diagnosis. Although the acute pharmacological actions of CCBs in the hearts are well-defined, little is known about the drug-specific effects on human cardiomyocyte transcriptomes and physiological alterations after long-term exposure.
objectiveThis study aimed to simulate chronic CCB treatment and to examine both the functional and transcriptomic changes in human cardiomyocytes. METHODS AND
resultsWe differentiated cardiomyocytes and generated engineered heart tissues from 3 human induced pluripotent stem cell lines and exposed them to 4 different CCBs-nifedipine, amlodipine, diltiazem, and verapamil-at their physiological serum concentrations for 2 weeks. Without inducing cell death and damage to myofilament structure, CCBs elicited line-specific inhibition on calcium kinetics and contractility. While all 4 CCBs exerted similar inhibition on calcium kinetics, verapamil applied the strongest inhibition on cardiomyocyte contractile function. By profiling cardiomyocyte transcriptome after CCB treatment, we identified little overlap in their transcriptome signatures. Verapamil is the only inhibitor that reduced the expression of contraction-related genes, such as MYH (myosin heavy chain) and troponin I, consistent with its depressive effects on contractile function. The reduction of these contraction-related genes may also explain the responsiveness of patients with hypertrophic cardiomyopathy to verapamil in managing left ventricular outflow tract obstruction.
conclusionsThis is the first study to identify the transcriptome signatures of different CCBs in human cardiomyocytes. The distinct gene expression patterns suggest that although the 4 inhibitors act on the same target, they may have distinct effects on normal cardiac cell physiology.
Indexed as
Identifiers
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.