Is there a role for oxidative stress and mitochondrial dysfunction in age-associated bladder disorders?

Millions of individuals worldwide are affected by age-related lower urinary tract symptoms (LUTSs), including impaired detrusor contractility, detrusor overactivity, decreased bladder sensation, as well as increased bladder capacity often resulting in incomplete bladder emptying. Yet, the underlying factors that contribute to these symptoms are not known and there are few therapies to treat these disorders. Because of the complex pathophysiology, a number of animal models have been studied over the years to better understand mechanisms underlying patient symptoms. Such animal models can aid in the investigation of aspects of age-associated LUTSs that cannot be pursued in humans as well as to develop and test potential therapies. In addition, the search for urinary factors that may be a causative agent has resulted in the discovery of a number of potential targets that could serve as predictive biomarkers which can aid in early diagnosis and treatment of these chronic disorders. Recent evidence has supported a role for chronic changes in mitochondrial function and oxidative stress (along with production of reactive oxygen species) and abnormal urodynamic behavior in older patients. This review discusses new insights into how aging alters fundamental cellular processes that impair signaling in the bladder wall, resulting in abnormal voiding function.