Benign prostatic hyperplasia nodules in patients treated with celecoxib and/or finasteride have reduced levels of NADH dehydrogenase [ubiquinone] iron-sulfur protein 3, a mitochondrial protein essential for efficient function of the electron transport chain.
Teresa T LiuTaro IgarashiNathalie El-KhouryNnamdi IhejirikaKelsey PaxtonJuliann JaumotteRajiv DhirChandler N HudsonJoel B NelsonDonald B DeFrancoNaoki YoshimuraZhou WangLaura E PascalPublished in: The Prostate (2024)
These findings suggest that celecoxib and/or finasteride are associated with an overall decrease in NDUFS3 levels in prostate tissues but do not impact the presence of inflammatory cells, suggesting a decline in mitochondrial CI function in the absence of enhanced inflammation. Given that BPH has recently been associated with increased prostatic mitochondrial dysfunction, celecoxib and/or finasteride may exacerbate existing mitochondrial dysfunction in some BPH patients thereby potentially limiting their overall efficacy in providing metabolic stability and symptom relief.
Keyphrases
- benign prostatic hyperplasia
- lower urinary tract symptoms
- oxidative stress
- induced apoptosis
- end stage renal disease
- ejection fraction
- newly diagnosed
- chronic kidney disease
- binding protein
- protein protein
- prognostic factors
- amino acid
- cell cycle arrest
- patient reported
- peritoneal dialysis
- patient reported outcomes
- cell death
- endoplasmic reticulum stress