Muscle Satellite Cell Activation

Injury & Signaling

Injury severity 50%

Activation signal (HGF/c-Met) 1.0×

Cell Fate Decision

Self-renewal probability r 35%

Proliferation rate 1.0×

Fusion speed 1.0×

Satellite Cell Pool

Quiescent (Pax7+)

Activated (MyoD+)

Differentiating

Fused into fiber

Fiber repair0%

Time since injury

—

Total pool

Quiescent stem (Pax7+) Activated / proliferating (MyoD+) Differentiating (fusing)

How it works

Satellite cells are adult muscle stem cells that sit quiescent between the sarcolemma and basal lamina of a myofiber, marked by the transcription factor Pax7. Injury releases HGF, which binds the c-Met receptor and, together with Notch/Wnt signaling, breaks quiescence.

dQ/dt = -a·S(t)·Q + 2·p·r·A
dA/dt =  a·S(t)·Q - p·A
dD/dt =  2·p·(1-r)·A - f·D
S(t)  =  exp(-t / τ)          (decaying injury signal)

Q = quiescent pool, A = activated/proliferating myoblasts (MyoD+), D = differentiation-committed cells fusing into the fiber. Each proliferating cell divides at rate p; on division, a fraction r of daughters returns to the quiescent state (self-renewal, keeping Pax7 high) while the rest commit to differentiation (Pax7 off, Myogenin on) and fuse, restoring the fiber. This stochastic, asymmetric-fate model (Kuang et al., 2007) is how the finite satellite-cell reserve survives repeated rounds of muscle damage instead of being exhausted by a single injury.

Injury severity — how much of the fiber is damaged, setting the activation radius and the fusion target for full repair.
Activation signal — strength of the HGF/c-Met chemical gradient driving Q → A transitions near the wound.
Self-renewal probability r — the fate-decision knob: low r drains the stem pool fast but repairs quickly; high r preserves the reserve for future injuries at the cost of slower repair.
Proliferation / fusion rate — how fast activated cells divide, and how fast committed cells fuse into the fiber.

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