Bio-actuators, as Biomedical Models for Dystrophies

We develop 3D bioprinted bioactuators that replicate human neuromuscular units to study Duchenne Muscular Dystrophy in a physiologically relevant setting. By capturing both muscle function and nerve–muscle communication, the platform enables investigation of disease mechanisms and testing of therapies that stabilize neuromuscular junctions. This approach aims to accelerate the development of targeted treatments to preserve muscle function and improve patient outcomes.

Duchenne Muscular Dystrophy (DMD) is a severe genetic disease characterized by progressive muscle degeneration and impaired communication between nerves and muscles. To better understand these processes, our project develops engineered bioactuators as advanced in vitro models of the neuromuscular unit.


In this FSRMM-funded project, we will use 3D bioprinting and fabricate living constructs that combine human muscle cells and motor neurons in a controlled architecture, closely replicating the neuromuscular junction (NMJ)—the critical interface where nerve signals trigger muscle contraction. Through extrusion-based bioprinting, we achieve spatially organized and distributed integration of both cell types, enabling more physiologically relevant models than conventional cultures.


These biohybrid systems allow us to study not only muscle weakness but also the stability and functionality of the neuromuscular connection, which is increasingly recognized as a key factor in DMD progression. By monitoring contractile activity and signal transmission, we can directly assess how the neuromuscular unit deteriorates and responds to interventions.


A central goal of this work is to identify and evaluate therapeutic strategies that improve NMJ stability. The platform will be used to test candidate drugs and biomolecular treatments, providing a scalable and human-relevant system for preclinical screening.


By combining tissue engineering, biofabrication, and neuromuscular biology, this project aims to advance our understanding of DMD and accelerate the development of targeted therapies that preserve muscle function and improve patient outcomes.

external page FSRMM Project Webpage

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