ArticleJournal of tissue engineering
Full-length dystrophin deficiency leads to contractile and calcium transient defects in human engineered heart tissues.
Article in Journal of tissue engineering. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Monitoring in real time and far-red imaging of HNature chemical biology · 2026Article
- Molecular Mechanisms and Therapeutic Strategies in Heart Failure Due to Dystrophin Deficiency: A Comprehensive Review.Reviews in cardiovascular medicine · 2026Review
- Current Trends in Duchenne Muscular Dystrophy Research and Therapy: 3D Cardiac Modelling.Journal of cachexia, sarcopenia and muscle · 2026Review
- Dystrophin Loss in Engineered Heart Tissues Recapitulates Clinically Relevant Aspects of Dystrophic Cardiomyopathy.Journal of biomechanical engineering · 2026Article
- Human Cardiac Organoids: Advances and Prospects from Construction to Preclinical Drug Evaluation.Cells · 2025Review
- Review
- Suspended Tissue Open Microfluidic Patterning (STOMP).Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Suspended Tissue Open Microfluidic Patterning (STOMP).bioRxiv : the preprint server for biology · 2025Article
- Three-Dimensional iPSC-Based In Vitro Cardiac Models for Biomedical and Pharmaceutical Research Applications.International journal of molecular sciences · 2024Review
- Incomplete-penetrant hypertrophic cardiomyopathyProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Right ventricular preload and afterload challenge induces contractile dysfunction and arrhythmia in isolated hearts of dystrophin-deficient male mice.Physiological reports · 2024Article
- Ultra-fast genetically encoded sensor for precise real-time monitoring of physiological and pathophysiological peroxide dynamics.Research square · 2024Article
- Structure-guided engineering of a fast genetically encoded sensor for real-time HbioRxiv : the preprint server for biology · 2024Article
- The new era of cardiovascular research: revolutionizing cardiovascular research with 3D models in a dish.Medical review (2021) · 2024Review
- PIV-MyoMonitor: an accessible particle image velocimetry-based software tool for advanced contractility assessment of cardiac organoids.Frontiers in bioengineering and biotechnology · 2024Article
- Modeling Duchenne Muscular Dystrophy Cardiomyopathy with Patients' Induced Pluripotent Stem-Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2023Review
- Calcium handling maturation and adaptation to increased substrate stiffness in human iPSC-derived cardiomyocytes: The impact of full-length dystrophin deficiency.Frontiers in physiology · 2022Article
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 2 institutions in 2 countries.
Funding
Abstract
Cardiomyopathy is currently the leading cause of death for patients with Duchenne muscular dystrophy (DMD), a severe neuromuscular disorder affecting young boys. Animal models have provided insight into the mechanisms by which dystrophin protein deficiency causes cardiomyopathy, but there remains a need to develop human models of DMD to validate pathogenic mechanisms and identify therapeutic targets. Here, we have developed human engineered heart tissues (EHTs) from CRISPR-edited, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) expressing a truncated dystrophin protein lacking part of the actin-binding domain. The 3D EHT platform enables direct measurement of contractile force, simultaneous monitoring of Ca
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.