Internal diseases and molecular mechanisms causing slipped capital femoral epiphysis in children

Figure 2 Molecular pathways potentially involved in the pathogenesis of slipped capital femoral epiphysis. NF-κB: Nuclear factor kappa B; FAK: Focal adhesion kinase; SOX9: SRY-box transcription factor 9; ROS: Reactive oxygen species; ROR2: Receptor tyrosine kinase-like orphan receptor 2; Rac1: Ras-related C3 botulinum toxin substrate 1; RhoA: Ras homolog family member A; ROCK: Rho-associated protein kinase; JNK: C-Jun N-terminal kinase; c-JUN: Cellular Jun N-terminal kinase substrate; AP-1: Activator protein 1.