In the last two decades,
nerve growth factor (
NGF), initially described as a prototypical trophic factor in the development of sensory and sympathetic innervation, has emerged as a complex regulator of neural plasticity along the micturition pathways. This review aims to summarize the current experimental and clinical evidence for a role of
NGF in urinary bladder. Experimental administration of
NGF elicits the states of increased sensation, urgency, and bladder
hyperreflexia, resembling pathologies associated with bladder overactivity and inflammatory
pain, such as
overactive bladder syndrome (OAB) and
interstitial cystitis/
painful bladder syndrome (IC/PBS). There is strong experimental evidence, including the effective therapeutic targeting, on the direct causal role of
NGF in rodent models of
bladder outlet obstruction,
spinal cord injury, diabetic bladder dysfunction, and interstitial
inflammation. In humans, there are attempts to employ urinary
NGF levels as a diagnostic marker in various forms of OAB and IC/PBS. In near future, use of novel experimental tools, such as urothelium-specific
NGF transgenic mice or more specific low-molecular weight
NGF receptor modulators, may provide better understanding of several unresolved issues in
NGF-related bladder dysfunction. Moreover, successful experimental therapeutic approaches, such as
NGF sequestering
proteins or modified
NGF antibodies, await the translation to the clinical treatment of bladder disorders.