Spinal cord injury–induced overflow incontinence reshapes the activin–follistatin–inhibin axis in mouse bladder and kidney

SCI reshapes the AFI axis in both bladder and kidney, characterized by coordinated but regionally distinct alterations in FST, INHA, INHBE, and INHBB expression. These findings extend the concept that the AFI axis contributes to urothelial-stromal homeostasis and suggest that AFI-axis remodeling is part of the molecular signature of neurogenic bladder and associated renal adaptation after SCI. These observational findings nominate the AFI axis as a priority pathway for future mechanistic and interventional evaluation, with therapeutic potential to be determined using objective functional endpoints.