Pathophysiological effect of bladder outlet obstruction on the urothelium

Abstract

Bladder outlet obstruction (BOO) and associated lower urinary tract symptoms are major urological issues that significantly affect patient's quality of life and may lead to severe complications. The prevalence of both is increasing each year, raising the burden to health system. Therefore, casual and symptomatic treatment should be of great importance. However, management of symptoms is often difficult as their pathophysiology is multifactorial and not well elucidated. Recently urothelium has gathered much attention as one of the potential causal agents. It has been suggested that in addition to its barrier function, urothelium regulates transport through blood-urine barrier and is a part of "sensory web" by which it modulates afferent input. In this review we focus on adjustment of urothelium related to BOO in terms of its ultrastructure, barrier and transport function, and impact on "sensory web."

M3 receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

“…Pathological tissue remodeling in bladders can be caused by BOO. These alterations include malfunction of urothelium, smooth muscle hypertrophy, and extracellular matrix (ECM) deposition that would result in LUTS, decreased bladder compliance, residual urine, and even dysfunction of the organ 4,5 . ECM accumulation is of great importance in the progression of BOO that can change the biomechanical properties of the bladder, leading to the transition from compensation to decompensation 6 …”

“…These alterations include malfunction of urothelium, smooth muscle hypertrophy, and extracellular matrix (ECM) deposition that would result in LUTS, decreased bladder compliance, residual urine, and even dysfunction of the organ. 4,5 ECM accumulation is of great importance in the progression of BOO that can change the biomechanical properties of the bladder, leading to the transition from compensation to decompensation. 6 Previous studies in chronic obstructive pulmonary diseases (COPD) and asthma, suggested that M receptors played an important role in the process of lung tissue remodeling.…”

Multi-Omics Characterization of Circular RNA-Encoded Novel Proteins Associated With Bladder Outlet Obstruction

“…Bladder outlet obstruction (BOO) is a urological condition featured by voiding difficulty, abdominal straining during voiding, increased postvoid residual and reduced urine flow rate due to increased detrusor pressure, and which is usually associated with lower urinary tract symptoms (LUTS) (Meier and Padmanabhan, 2016;Niemczyk et al, 2018). The prevalence of BOO was previously predicted to be as high as 21.8% among population aged over 20 years, which is affecting more than one billion patients worldwide (Niemczyk et al, 2018).…”

“…Bladder outlet obstruction (BOO) is a urological condition featured by voiding difficulty, abdominal straining during voiding, increased postvoid residual and reduced urine flow rate due to increased detrusor pressure, and which is usually associated with lower urinary tract symptoms (LUTS) (Meier and Padmanabhan, 2016;Niemczyk et al, 2018). The prevalence of BOO was previously predicted to be as high as 21.8% among population aged over 20 years, which is affecting more than one billion patients worldwide (Niemczyk et al, 2018). It is known that BOO pathogenesis could be induced by anatomic factors including benign prostatic obstruction (BPO), pelvic organ prolapses, stricture diseases, urologic malignancies and iatrogenic obstruction, as well as functional causes such as dysfunctional voiding, primary bladder neck obstruction, and Fowler's syndrome (King and Goldman, 2014;Meier and Padmanabhan, 2016;Fusco et al, 2018).…”

Upregulation of AQP2 mediated by transcription factor FOXO1 inhibits TGF‑β‑induced fibrosis in human urothelial cells

“…Long-term BOO may result in bladder structure remodeling and bladder detrusor muscle dysfunction, which may in turn lead to a series of urinary tract symptoms, including frequent urination, urination urgency and urinary incontinence, severely compromising the quality of life of the patients ( 2 ). Currently, BOO affects ~1.1 billion individuals worldwide, with the occurrence of BOO and associated lower urinary tract symptoms increasing annually ( 3 , 4 ). During the pathological process of BOO, smooth muscle hypertrophy occurs in an attempt to overcome the increased urethral resistance, which leads to the eventual decompensation to fibrosis ( 5 ).…”