Skeletal Muscle Disease Modeling

Mechanistic analysis of Duchenne muscular dystrophy and muscle damage susceptibility

From dystrophin loss to tissue-level mechanical damage

Duchenne muscular dystrophy changes how force is transmitted through muscle tissue. Using a multiscale muscle modeling framework, FilamenTech examined how the lack of dystrophin affects extracellular matrix deformation between fast and slow muscle fibers.

Key findings:

1
Modeled how loss of dystrophin changes mechanical coupling between neighboring fibers.
2
Estimated elevated shear strain in extracellular matrix regions between fast and slow fibers.
3
Linked strain patterns to local micro-injury, inflammation, and progressive degeneration.
4
Demonstrated how multiscale modeling can support therapeutic research in neuromuscular disease.

This case study extends FilamenTech’s platform logic beyond cardiac muscle, showing how mechanistic modeling can reveal tissue-level consequences of molecular defects in Duchenne muscular dystrophy.

Reference:
Prodanovic et al., BIBE 2021

Scientific work:

Prodanovic et al., BIBE 2021
Structural schematic of skeletal muscle showing the sarcomere components (F-actin, F-myosin, nebulin, titin), sarcolemma, dystrophin, and glycoprotein complex connecting the contractile apparatus to the extracellular matrix. This architecture forms the basis of the MUSICO multi-fiber model, which explicitly includes the mechanical role of dystrophin in transmitting forces between sarcomeres and the cell membrane.
MUSICO multi-fiber model setup incorporating the Huxley 2-state kinetic scheme with Ca²⁺ regulation, applied to a tissue cross-section containing fast (α) and slow (β) skeletal muscle fibers embedded in extracellular matrix with and without dystrophin. The model captures the mechanical coupling between fiber types and the extracellular matrix at physiologically relevant fiber dimensions.
MUSICO-predicted shear strain maps in skeletal muscle cross-sections during loaded contraction with dystrophin present (A) and absent (B, DMD condition). Loss of dystrophin results in markedly elevated and heterogeneous shear strain at the fiber-matrix interface, consistent with the hypothesis that membrane damage in DMD is driven by excessive shear forces generated during contraction.
Tension transients predicted by MUSICO (dashed) and the multi-scale finite element model (solid) for fast and slow skeletal muscle fibers under isometric and light-loading conditions. MUSICO sarcomere-level predictions are directionally consistent with the multi-scale FE results, validating the mechanistic framework for skeletal muscle contraction across both fiber types.
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