Targeting neurotrophin and nitric oxide signaling to promote recovery and ameliorate neurogenic bladder dysfunction following spinal cord injury -Mechanistic concepts and clinical implications

This review summarizes a workshop on targeting neurotrophin and nitric oxide signaling to improve neurogenic bladder dysfunction after spinal cord injury (SCI). SCI causes impaired mobility, neurogenic detrusor overactivity (NDO), detrusor sphincter dyssynergia (DSD), and reduced quality of life. The workshop explored therapeutic agents to reduce SCI lesions and manage lower urinary tract (LUT) changes. Potential agents included LM11A-3 (p75 neurotrophin receptor modulator), LM22B-10 (Trk receptor target), and cinaciguat (sGC activator). Bladder targets discussed included purinergic pathways, afferent signaling, and fibrosis. The importance of mechanosensitive signaling in DSD and potential drug targets were also highlighted, emphasizing restoration of function over normal function downregulation.

A J Kanai, K.-E Andersson, C H Fry, N Yoshimura