Anxiety‑induced overactive bladder: The role of oxidative stress and NF‑κB signaling pathway with Hsp90 as a potential biomarker

Overactive bladder (OAB) is a common condition that affects lower urinary tract symptoms and markedly affects the physical and mental health of individuals. While the cause of OAB is unclear, some studies suggest a possible link to psychological factors, particularly anxiety. Despite this, research on the connection between anxiety and OAB is limited. The present study aimed to explore anxiety‑induced OAB by analyzing clinical data and identifying key genes and pathways in vivo, ultimately providing new insights for diagnosing and treating OAB. Clinical data were analyzed to explore the relationship between anxiety and OAB. A chronic restraint stress model was used to induce anxiety, with histological scoring and cystometry assessing bladder function. Bladder transcriptomics identified key genes and pathways in OAB development. Differences in oxidative stress and NF‑κB pathway activity were validated using immunohistochemistry, enzyme‑linked immunosorbent assay and quantitative PCR. Clinical data showed a positive link between overactive bladder symptom scores and general anxiety disorder scale‑7, with higher urination urgency scores in OAB patients with anxiety. Analysis confirmed anxiety as an independent risk factor for OAB. In vivo experiments showed that anxiety induced OAB‑like symptoms in mice through oxidative stress and NF‑κB pathway activation, with RNA sequencing revealing key hub genes included heat shock protein 90 (Hsp90) aa1, Hsp90ab1 and Hsp90b1. The present study demonstrated that anxiety may precipitate the onset of OAB by activating oxidative stress and the NF‑κB signaling pathway. Hsp90 may serve as a potential biomarker for diagnosing anxiety‑induced OAB. Retrospectively registered on 1 April 2025, The present study received the identifier ChiCTR2500100548 from the Chinese Clinical Trial Registry.