ArticleAdvanced healthcare materials2026
Patient-Derived 3D Bioprinted Cardiac Organoid Constructs Reveal Key Pathological Features of Duchenne Muscular Dystrophy.
Article in Advanced healthcare materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Human cardiovascular organoids: Biomedical applications and ethical challenges.American heart journal plus : cardiology research and practice · 2026Review
- Stem cell-based regenerative therapies for non-ischemic cardiomyopathy: mechanistic insights, clinical evidence, and future directions.Molecular biology reports · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a genetic disorder characterized by progressive muscle degeneration that significantly reduces the quality of life and lifespan of patients. Currently, cardiomyopathy represents the leading cause of death in later stages of the disease. While calcium dysregulation, fibrosis, and fat deposits are well-documented hallmarks of DMD cardiomyopathies, the exact pathogenic mechanisms remain unclear due to the lack of reliable models. In this study, we developed 3D cardiac organoids (COs) from DMD patient-derived induced pluripotent stem cells (DMD-hiPSCs), their isogenic control (DMD-Iso-hiPSCs), and a healthy hiPSC line (HC-hiPSCs). By day 15 of cardiac differentiation, DMD-COs exhibited key disease features, including increased cell death, elevated ROS levels, and calcium signaling defects, compared with controls. Leveraging bioprinting technology, COs were embedded in a 7% alginate-5% gelatin hydrogel to generate bioprinted constructs (HC-bCOs, DMD-Iso-bCOs, and DMD-bCOs). These constructs self-organized, displaying increased cell-cell communication, and reduced levels of the early cardiac transcription factor NKX2.5. By day 14 post-bioprinting, DMD-bCOs showed increased cell death and dysregulated expression of cardiac and fibrotic markers, mimicking DMD-associated cardiomyopathy. This study demonstrates the potential of both COs and bCOs as a tool for studying DMD cardiomyopathy and advancing drug screening and therapies.
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Registered trials
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