ArticleNature cell biology2016
iPSC-derived cardiomyocytes reveal abnormal TGF-β signalling in left ventricular non-compaction cardiomyopathy.
Article in Nature cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 2 of them syntheses 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
120 citing papers in PubMed, 2 syntheses or guidelines pooled it, 171 citations in OpenAlex.
- Pooled it
- Clinical and genetic insights into non-compaction: a meta-analysis and systematic review on 7598 individuals.Clinical research in cardiology : official journal of the German Cardiac Society · 2019Pooled it
- Emerging Technologies in Cardiovascular Disease Modeling: Bridging Basic Science and Clinical Translation.Cells · 2026Review
- PRDM16 as a Multifaceted Pharmacological Target in Kidney Diseases: From Epigenetic Mechanisms to Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Rethinking Left Ventricular Noncompaction and Excessive Left Ventricular Trabeculation: Development, Genetics, and a Proposed Conceptual Framework.Journal of clinical medicine · 2026Review
- PRDM16 modulates aspects of cell cycle dynamics and maturation in human iPSC-derived cardiomyocytes.Stem cell reports · 2026Article
- Hypoplastic Left Heart Syndrome Cardiomyocytes Exhibit Intrinsic Stress Vulnerabilities and Augmented Stress Responses in vitro.Stem cell reviews and reports · 2026Article
- PRDM16, a new kid on the block in cardiovascular health and disease.Cardiovascular research · 2025Review
- Gastruloids enable modeling of the earliest stages of human cardiac and hepatic vascularization.Science (New York, N.Y.) · 2025Article
- Induced Pluripotent Stem Cells in Cardiomyopathy: Advancing Disease Modeling, Therapeutic Development, and Regenerative Therapy.International journal of molecular sciences · 2025Review
- ARID5A orchestrates cardiac aging and inflammation through MAVS mRNA stabilization.Nature cardiovascular research · 2025Article
- Methods for Generating Self-Organizing Human Patterned Heart Organoids Using Pluripotent Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- PRDM16 determines specification of ventricular cardiomyocytes by suppressing alternative cell fates.Life science alliance · 2024Article
- Review
- Clinical trials in-a-dish for cardiovascular medicine.European heart journal · 2024Review
- Cardiomyocyte proliferation and regeneration in congenital heart disease.Pediatric discovery · 2024Article
- Advances in induced pluripotent stem cell-derived cardiac myocytes: technological breakthroughs, key discoveries and new applications.The Journal of physiology · 2024Review
- Endocardial HDAC3 is required for myocardial trabeculation.Nature communications · 2024Article
- HOIL-1L deficiency induces cell cycle alteration which causes immaturity of skeletal muscle and cardiomyocytes.Scientific reports · 2024Article
- Cardiac manifestations of human ACTA2 variants recapitulated in a zebrafish model.Journal of human genetics · 2024Article
60 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
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Left ventricular non-compaction (LVNC) is the third most prevalent cardiomyopathy in children and its pathogenesis has been associated with the developmental defect of the embryonic myocardium. We show that patient-specific induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) generated from LVNC patients carrying a mutation in the cardiac transcription factor TBX20 recapitulate a key aspect of the pathological phenotype at the single-cell level and this was associated with perturbed transforming growth factor beta (TGF-β) signalling. LVNC iPSC-CMs have decreased proliferative capacity due to abnormal activation of TGF-β signalling. TBX20 regulates the expression of TGF-β signalling modifiers including one known to be a genetic cause of LVNC, PRDM16, and genome editing of PRDM16 caused proliferation defects in iPSC-CMs. Inhibition of TGF-β signalling and genome correction of the TBX20 mutation were sufficient to reverse the disease phenotype. Our study demonstrates that iPSC-CMs are a useful tool for the exploration of pathological mechanisms underlying poorly understood cardiomyopathies including LVNC.
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.