Collagen content in the bladder of men with LUTS undergoing open prostatectomy: A pilot study

Self Cite

Studies on bladder dysfunction (BD), more specifically functional‐urodynamic changes in the bladder as a result of bladder outlet obstruction (BOO) have been summarized for this TT. Based on available, but limited evidence from human studies a three‐stage model can be hypothesized to characterize BOO‐induced bladder remodeling: hypertrophy, compensation (increased detrusor contractility during the voiding phase, often in combination with filling phase detrusor overactivity) followed by the phase of decompensation [detrusor underactivity]. The time between the start of compensation and eventual decompensation seems to be determined by age of onset, severity, and type of obstruction and clinical mitigating factors such as vascular and metabolic problems. Understanding the relative contributions of these factors may allow the development of personalized timelines and probabilities for these obstructed patients.

Section: What Is the Role Of Clinical Mitigating Factors?mentioning

confidence: 86%

Section: How Might Boo Lead To Bd and More Particularly What Is The Bmentioning

confidence: 99%

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Do functional changes occur in the bladder due to bladder outlet obstruction? ‐ ICI‐RS 2018

Bosch

Abrams

Averbeck

et al. 2019

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“…Severe BOO has been found to be associated with increased oxidative stress in the bladder wall of men with lower urinary tract symptoms (LUTS) . Furthermore, collagen content was found to be higher in the bladder wall of males with LUTS and increased postvoid residual urine and reduced compliance . As a result of BOO, the bladder may ultimately become noncompliant, characterized by small functional capacity and increased intravesical storage pressure.…”

Section: Scs For Bladder Dysfunction Related To Boomentioning

confidence: 99%

“…44 Furthermore, collagen content was found to be higher in the bladder wall of males with LUTS and increased postvoid residual urine and reduced compliance. 45 As a result of BOO, the bladder may ultimately become noncompliant, characterized by small functional capacity and increased intravesical storage pressure. Various parameters, such as mechanical strain, bladder wall hypoxia, and oxidative stress and inflammation have been implicated in the pathogenesis of BOO-associated LUTD.…”

Section: Dysfunction Related To Boomentioning

confidence: 99%

Stem cells and lower urinary tract dysfunction: Has its potential finally reached clinical maturity? ICI‐RS2018

Chermansky

Mitsogiannis

Abrams

et al. 2019

Aims: Efforts to engineer and repair genitourinary tissue to treat lower urinary tract dysfunction (LUTD) have recently increased thanks in part to advances in stem cell (SC) research. At the International Consultation on Incontinence-Research Society meeting in Bristol in 2018 a proposal was convened to address the question: has the potential of SCs in treating LUTD reached clinical maturity? Methods: The proposal conducted a literature review and an expert consensus meeting focusing on available data from animal models and clinical trials involving the use of SCs for LUTD. Results: To date, there are only small studies investigating bladder replacement using scaffolds with or without SC. Results have been conflicting because of the variability in cell numbers, biomaterials types, and graft surface differences. Similarly, preclinical results suggest a possible role of SC in bladder outlet obstruction (BOO); however, SC clinical trials for BOO are lacking. Research into the use of SC for female stress urinary incontinence (SUI) is close to reaching clinical maturity. In the Canadian phase 3 randomized controlled trial (RCT), a beneficial effect of adult muscle-derived cells (AMDC) over placebo was detected in reducing the frequency of incontinence episodes, especially after prior anti-incontinence surgery. Only two small studies have been published on male SUI.Conclusions: Questions remain regarding the mechanism of action of SC injected into the LUT and the viability of cells seeded onto grafts placed into the LUT. Also, the optimal time for intervention with SC therapy in the LUT remains to be elucidated. K E Y W O R D Sbladder, bladder outlet obstruction, incontinence, neurogenic, regenerative, stem cells

The preventive effects of colony‐stimulating factor 1 receptor (CSF‐1R) inhibition on bladder outlet obstruction induced remodeling

Wang

Sun

Gao

et al. 2022

Introduction Bladder outlet obstruction (BOO) is a common problem that can affect bladder structure and function. Currently, there is no effective drugs available to prevent BOO‐induced remodeling. Previous reports have demonstrated that the pathogenesis of BOO is associated with macrophage infiltration and polarization, which is physiologically dependent on colony‐stimulating factor 1 receptor (CSF‐1R) activation. Here we utilized a highly selective CSF‐1R inhibitor, GW2580, to determine its preventive effects on BOO‐induced remodeling. Methods A total of 24 Sprague–Dawley rats were randomly divided into sham, BOO + vehicle, and BOO + GW2580 group. GW2580 or vehicle control was administrated by oral gavage at daily doses of 40 mg/kg for 6 weeks. Bladder samples were collected for histopathology, immunohistochemistry, immunofluorescence, western blotting, and flow cytometry analysis. Results Our results demonstrated that bladder fibrosis was ameliorated by GW2580 compared with the vehicle group (22.01% ± 5.13% vs. 32.15% ± 7.24%, p < 0.01). Furthermore, treatment with GW2580 induced an inhibition of macrophage infiltration (4.41% ± 1.28% vs. 13.57% ± 3.42%, p < 0.001) and M2 macrophage polarization (10.67% ± 4.15% vs. 28.59% ± 6.38%, p < 0.001). There was also a decrease of profibrotic F4/80+ α‐smooth muscle actin+ (α‐SMA+) macrophage to myofibroblast transition (9.11% ± 2.58% vs. 17.33% ± 4.01%, p < 0.001) and CD163+TGF‐β1+ cells (7.68% ± 2.10% vs. 14.17% ± 4.09%, p < 0.01) in the GW2580 group when compared with the vehicle group. Conclusions In summary, our findings showed that GW2580 is a worthwhile candidate for a follow‐up study to test in the treatment of BOO‐induced remodeling.