ArticleCommunications biology2025
Tissue-engineered neuromuscular organoids.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Human neuromuscular organoids mimic cancer-induced muscle cachexia.Cell reports methods · 2026Article
- Animal models of benign airway stenosis: Advances in construction techniques, evaluation systems, and perspectives.Animal models and experimental medicine · 2026Review
- Organoids for disease modeling and treatment: state-of-the-art.Experimental hematology & oncology · 2026Review
- Innovations in skeletal muscle regeneration: from physiology to bioengineering approaches for repair and restoration.Frontiers in physiology · 2026Review
- Human Multi-Organ-on-a-Chip Platforms for Next-Generation Drug Delivery Strategies.Theranostics · 2026Review
- Novel Translational Concept: Axon-to-Muscle Exosomal Signaling as an Emerging Therapeutic Target in Spinal Muscular Atrophy.Biomedicines · 2025Review
- Engineering Assembloids to Mimic Graft-Host Skeletal Muscle Interaction.Advanced healthcare materials · 2025Article
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26 authors.
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Abstract
Skeletal muscle development, homeostasis, and function rely on complex interactions among multiple cell types and the extracellular matrix (ECM). Developing in vitro models that recapitulate both intrinsic cellular and extrinsic ECM elements of innervated skeletal muscle is crucial for advancing basic biology and disease modeling studies. Here, we combine tissue engineering approaches with human induced pluripotent stem cell (hiPSC) technology to create tissue-engineered neuromuscular organoids (t-NMOs). Using decellularized muscles as scaffolds, hiPSCs differentiate to form organoids that establish a continuum with the provided biomaterial. After 30 days, t-NMOs exhibit compartmentalized neural and muscular components that establish functional interactions, allowing muscle contraction. We demonstrate the model's potential by creating Duchenne Muscular Dystrophy patient-specific t-NMOs, that recapitulate the reduced skeletal muscle contraction and altered calcium dynamics typical of the disease. Altogether, our study presents a tissue-engineered organoid that model the human neuromuscular system (dys)function, highlighting the potential of applying the ECM in organoid engineering.
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