# Examining the role of defective oxidative phosphorylation in the normal and diseased prostate

> **NIH NIH F31** · UNIVERSITY OF WISCONSIN-MADISON · 2024 · $38,608

## Abstract

ABSTRACT
Lower urinary tract symptoms (LUTS) are a significant burden to aging men and are often as a result of benign
prostatic hyperplasia (BPH). While BPH/LUTS is not commonly fatal with proper medical intervention, it does
cause a significant reduction in quality of life for many men as they age. Furthermore, BPH/LUTS increases risk
of mortality and results in billions of dollars in healthcare costs annually. There is currently a subset of BPH/LUTS
patients that fail FDA-approved treatments (α-blockers, 5ARI), and these patients have been shown to have
increased prostatic fibrosis. There is no FDA-approved medication targeting fibrosis or the aging process in
BPH/LUTS, even though aging is the greatest risk factor. This proposal aims to develop a better understanding
about the role of aging, fibrosis, and mitochondrial dysfunction in BPH/LUTS. Mitochondrial dysfunction is a
hallmark of both aging and fibrosis and has not been thoroughly studied in relation to BPH/LUTS. Preliminary
data suggests that oxidative phosphorylation (OXPHOS) is a mitochondrial pathway contributing to cellular
dysfunction in BPH/LUTS. Aim 1 of this proposal intends to investigate the connection between OXPHOS
disruption and lower urinary tract dysfunction (LUTD) in a novel mouse model. Aim 2 of this proposal will
investigate the connection between OXPHOS disruption and pathways associated with fibrosis, using genetic
loss-of-function cell line models. Finally, Aim 3 will work to identify a new pathway of interest for treatment, using
oleic acid as a mitochondrial metabolism modulator. Collectively, these aims will improve our overall
understanding of the processes underlying BPH/LUTS, with a special focus on aging, mitochondrial dysfunction,
and fibrosis. This proposal hopes to provide translational outcomes that can eventually improve patient care and
treatment options.

## Key facts

- **NIH application ID:** 10816415
- **Project number:** 5F31DK136335-02
- **Recipient organization:** UNIVERSITY OF WISCONSIN-MADISON
- **Principal Investigator:** Alexis Elizabeth Adrian
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $38,608
- **Award type:** 5
- **Project period:** 2023-04-01 → 2026-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10816415

## Citation

> US National Institutes of Health, RePORTER application 10816415, Examining the role of defective oxidative phosphorylation in the normal and diseased prostate (5F31DK136335-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10816415. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*