Abstract: Diabetic bladder dysfunction (DBD) is the most common chronic complication of diabetes mellitus in urology. Approximately 40%-60% of diabetic patients are troubled by DBD, presenting with varying degrees of lower urinary tract symptoms, mainly including reduced bladder filling sensation, detrusor contractile dysfunction, increased bladder capacity and elevated post-void residual urine volume, which seriously affect patients’ quality of life. The pathophysiology of DBD involves abnormal detrusor status, urothelial dysfunction, and neuropathy. As the structural basis for bladder emptying, changes in the structure and function of the detrusor are key to the occurrence and development of DBD. This review focuses on the time-dependent changes of the detrusor during the course of DBD, systematically expounds the dynamic evolution law from compensatory hyperactivity to decompensated hypoactivity, and deeply analyzes the core mechanisms driving the transition. In the early stage, compensation is dominated by increased neurotransmitter release, sensitization of purinergic signaling pathways and enhancement of calcium signaling pathways; With the progression of the disease, insulin signaling pathway disorders and lipid metabolism disorders drive smooth muscle phenotype transformation; Ultimately, comprehensive activation of oxidative stress leads to irreversible structural damage and functional failure of the detrusor.

Key words: diabetes mellitus, diabetic bladder dysfunction, detrusor, pathogenesis, animal models