Interstitial cystitis/bladder pain syndrome (IC/BPS) is characterized by bladder and/or pelvic pain, increased urinary urgency and frequency and nocturia. The pathophysiology of IC/BPS is poorly understood, and theories include chronic inflammation, autoimmune dysregulation, bacterial cystitis, urothelial dysfunction, deficiency of the glycosaminoglycan (GAG) barrier and urine cytotoxicity. Multiple treatment options exist, including behavioural interventions, oral medications, intravesical instillations and procedures such as hydrodistension; however, many clinical trials fail, and patients experience an unsatisfactory treatment response, likely owing to IC/BPS phenotype heterogeneity and the use of non-targeted interventions. Oxidative stress is implicated in the pathogenesis of IC/BPS as reactive oxygen species impair bladder function via their involvement in multiple molecular mechanisms. Kinase signalling pathways, nociceptive receptors, mast-cell activation, urothelial dysregulation and circadian rhythm disturbance have all been linked to reactive oxygen species and IC/BPS. However, further research is necessary to fully uncover the role of oxidative stress in the pathways driving IC/BPS pathogenesis. The development of new models in which these pathways can be manipulated will aid this research and enable further investigation of promising therapeutic targets.

间质性膀胱炎/膀胱疼痛综合征 (IC/BPS) 的特点是膀胱和/或盆腔疼痛、尿急、尿频和夜尿增多。 IC/BPS 的病理生理学目前尚不清楚，理论包括慢性炎症、自身免疫失调、细菌性膀胱炎、尿路上皮功能障碍、糖胺聚糖 (GAG) 屏障缺陷和尿液细胞毒性。存在多种治疗选择，包括行为干预、口服药物、膀胱灌注和水扩张等手术；然而，许多临床试验失败了，患者的治疗反应不令人满意，这可能是由于 IC/BPS 表型异质性和非靶向干预措施的使用。氧化应激与 IC/BPS 的发病机制有关，因为活性氧通过参与多种分子机制损害膀胱功能。激酶信号通路、伤害性受体、肥大细胞激活、尿路上皮失调和昼夜节律紊乱都与活性氧和 IC/BPS 有关。然而，还需要进一步的研究来充分揭示氧化应激在驱动 IC/BPS 发病机制中的作用。可以操纵这些途径的新模型的开发将有助于这项研究，并能够进一步研究有希望的治疗靶点。