Oxidative stress in bladder outlet obstruction: a narrative review.

BACKGROUND AND OBJECTIVE: Partial bladder outlet obstruction (pBOO) is a common urological disorder characterized by impaired urinary flow and elevated intravesical pressure, usually resulting from benign prostatic hyperplasia (BPH), urethral stricture, or other obstructive pathologies. pBOO induces progressive bladder dysfunction (BD) through complex mechanisms, in which oxidative stress (OS) plays an important role. This review aims to systematically elucidate the role of reactive oxygen species (ROS) and related signaling pathways in the pathogenesis of pBOO-induced BD, and summarize emerging therapeutic strategies targeting oxidative injury. METHODS: We conducted a comprehensive literature search using PubMed, Web of Science and China National Knowledge Infrastructure (CNKI) databases from October 1990 to April 2026. Key search terms included "Urinary Bladder Neck Obstruction", "Reperfusion Injury", "Oxidative Stress", "Hypoxia", and "Reactive Oxygen Species". Articles were screened for relevance to oxidative mechanisms in pBOO. Supplementary studies on OS signaling pathways were incorporated to enrich the mechanistic discussion. The selected studies were summarized and analyzed. As this study was designed as a narrative rather than a systematic review, no PRISMA flow diagram, standardized risk-of-bias assessment, or hierarchical evidence grading was performed. KEY CONTENT AND FINDINGS: pBOO triggers cyclic ischemia-reperfusion injury, leading to excessive ROS generation from enzymatic sources, mitochondrial dysfunction, and inflammatory activation. OS promotes BD through lipid peroxidation, protein carbonylation, DNA damage, activation of apoptosis, pyroptosis, and autophagy, and activation of multiple signaling pathways. Key signaling cascades involve ROS-nuclear factor kappa-B (NF-κB) inflammation signaling pathway, nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) antioxidant defense, mitochondrial permeability transition, and transforming growth factor beta (TGF-β)-mediated fibrosis. Several antioxidants and targeted agents have demonstrated efficacy in preclinical models by mitigating oxidative damage and improving bladder function. CONCLUSIONS: OS plays a critical role in the progression of pBOO-induced BD. Despite advances in understanding ROS-related mechanisms, clinical translation remains challenging due to the complexity of redox signaling. Future research should focus on defining precise molecular pathways, identifying biomarkers of oxidative injury, and developing multi-target therapies to restore redox homeostasis. Personalized approaches combining antioxidants with conventional treatments may improve outcomes for patients with refractory BD.