Our research will focus on peroxisome-proliferator activated receptor-gamma (PPARγ), inflammation and BPH/LUTS. We will look for links between inflammation and LUTS characterized by prostatic enlargement and changes in bladder biology associated with outflow obstruction. If links are found, we can then assess whether these diseases can be addressed by treatment and therapies aimed at PPARγ signaling and related pathways.
PPARγ activity plays a key role in normal prostate and bladder biology and function, and that loss of PPARγ activity contributes to inflammation and prostatic enlargement. We further hypothesize that PPARγ agonists can act to modify this response.
Determine if prostatic hyperplasia resulting from loss of PPARγ activity is a secondary consequence of prostatic inflammation rather than a primary effect of loss of PPARγ function.
Determine if PPARγ plays a critical role in the development of bladder function and the ability of the bladder to respond to bladder outlet obstruction.
Determine if diabetic patients receiving PPARγ agonists, prescribed to treat their diabetes, will progress more slowly to BPH/LUTS-related endpoints than patients treated by other means.