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

Figure 1 Primary internal diseases associated with slipped capital femoral epiphysis. NF-κB: Nuclear factor kappa B; IGF1: Insulin-like growth factor 1; GH-IGF-1: Growth Hormone-insulin-like growth factor-1 axis; CKD: Chronic kidney disease; MBD: Mineral and bone disorder; SCFE: Slipped capital femoral epiphysis; TSH: Thyroid-stimulating hormone; FSH: Follicle-stimulating hormone; LH: Luteinizing hormone.

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.