Urinary CTGF in Benign Prostatic Obstruction

Benign Prostatic Hyperplasia, Bladder Outlet Obstruction, Lower Urinary Tract Symptom

Benign prostatic obstruction (BPO) is one of the most common causes of bladder outlet obstruction (BOO) and may lead to progressive structural and functional alterations in the bladder over time. Prolonged obstruction triggers a bladder remodeling process characterized by detrusor hypertrophy, ischemia-reperfusion injury, smooth muscle loss, and progressive fibrosis. These pathological changes may result in impaired detrusor contractility, increased post-void residual volume, and suboptimal functional recovery following surgical treatment. Connective tissue growth factor (CTGF) is a matricellular protein that plays a key role in fibrogenesis and is markedly upregulated under hypoxic, ischemia-reperfusion, and inflammatory conditions. Experimental and cellular studies have demonstrated that CTGF promotes fibroblast proliferation, extracellular matrix production, and collagen deposition, thereby contributing to bladder fibrosis. Increased CTGF expression has also been associated with fibrotic differentiation of bladder smooth muscle cells. The aim of this observational study is to evaluate the relationship between urinary CTGF levels, bladder fibrosis, and functional response to surgical treatment in patients with benign prostatic obstruction. Preoperative urinary CTGF levels will be assessed and correlated with postoperative functional outcomes and clinical improvement. This study aims to determine whether urinary CTGF may serve as a non-invasive biomarker of bladder fibrosis and a potential predictor of surgical treatment response in patients with BPO.

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