Fig. 9. Hypothetical model for enhanced store-operated Ca²⁺ entry in dystrophic skeletal muscle fibers. In skeletal muscle, ryanodine receptors (RyR) are allosterically activated by L-type voltage-gated Ca²⁺ channels (VGCC) when plasma membrane (PM) is depolarized (V). SR Ca²⁺ released through ryanodine receptors triggers contraction and Ca²⁺ is pumped back into the SR by the SERCA. Ca²⁺-store depletion occurring during Ca²⁺ release through ryanodine receptors or when SERCA is blocked by thapsigargin triggers iPLA₂ activation, possibly by the release of calcium influx factor (CIF). Hydrolysis products of iPLA₂ (most likely lysophospholipids) may be responsible for SOC stimulation and Ca²⁺ influx. Overexpression of iPLA₂ in dystrophic muscle is likely to be responsible for enhanced Ca²⁺ influx through SOC.