title: [Physiopathology of overactive bladder syndrome].
abstract: The pathophysiology of OAB is complex, multifactorial and still largely unknown. Several pathophysiological mechanisms have been highlighted that may play a different role in different patient groups. There are now experimental evidences that support both the myogenic and neurogenic hypothesis, but in recent years the "integrative" hypothesis has been gaining more and more acceptance, where a disruption in the multiple interactions between different cell types (neurons, urothelium, interstitial cells, myocytes) and network functions represent a central element of lower urinary tract dysfunctions.  Of utmost importance, a disorder in the urothelial sensory function and in the urothelial/suburothelial non-neural cholinergic system, favored by age and comorbidities, appears to be crucial for the development of the OAB. Neuroplastic and detrusor changes in OAB are broadly similar to those observed in bladders exposed to outlet obstruction, neuropathies, inflammation or aging, and may be driven by a common urothelial dysfunction. Several signaling substances and their receptors were found to be involved in central pathways of bidirectional communication between the different cell types in the bladder, and were shown to be modified in several animal models of OAB as well as in human models, indicating new potential therapeutic targets.
authors.affiliation: Clinica Urologica, Dipartimento di Scienze chirurgiche, Policlinico Agostino Gemelli, Università Cattolica del Sacro Cuore, Roma, Italia. emilio.sacco@gmail.com
authors.forename: Emilio
authors.initials: E
authors.lastname: Sacco
mesh_terms: D000818:Animals; D002490:Central Nervous System / Q000503:physiopathology; D015897:Comorbidity; D003556:Cystitis / Q000503:physiopathology; D006801:Humans; D008160:Lumbosacral Plexus / Q000503:physiopathology; D008959:Models, Neurological; D009130:Muscle, Smooth / Q000473:pathology / Q000503:physiopathology; D058628:Myofibroblasts / Q000502:physiology; D020932:Nerve Growth Factor / Q000502:physiology; D009473:Neuronal Plasticity; D018377:Neurotransmitter Agents / Q000502:physiology; D017981:Receptors, Neurotransmitter / Q000502:physiology; D012018:Reflex / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013045:Species Specificity; D013119:Spinal Cord Injuries / Q000503:physiopathology; D001743:Urinary Bladder / Q000294:innervation; D001748:Urinary Bladder Neck Obstruction / Q000503:physiopathology; D053201:Urinary Bladder, Overactive / Q000503:physiopathology* / Q000601:surgery; D014554:Urination / Q000502:physiology; D019459:Urothelium / Q000503:physiopathology; D054460:rho-Associated Kinases / Q000502:physiology
chemical_list: D018377:Neurotransmitter Agents; D017981:Receptors, Neurotransmitter; D020932:Nerve Growth Factor; D054460:rho-Associated Kinases