# A Digital Twin for Designing Bladder Treatment informed by Bladder Outlet Obstruction Mechanobiology (BOOM)

> **NIH NIH R01** · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · 2024 · $614,430

## Abstract

Prostate enlargement arising from benign prostate hyperplasia (BPH) can constrict the urethra, causing bladder
outlet obstruction (BOO), a major contributing factor to the lower urinary tract symptoms (LUTS) that affect aging
men. The BOO bladder is capable of generating the elevated pressures necessary to overcome the rise in outlet
resistance and void through an increase in bladder smooth muscle cell mass. However, prolonged elevation in
voiding pressures induces progressive mechanobiological changes to the bladder wall that lead to LUTS,
including storage and voiding dysfunction. With rising numbers of BPH worldwide, prostate surgery to treat BOO
will increase in frequency. Therefore, there is an urgent need to understand why 30% of prostrate surgeries to
treat BOO are ineffective at resolving LUTS and to identify more effective treatment strategies.
We believe the reason for this gap in knowledge is that insufficient attention has been given to understanding
the coupling between changes to the bladder wall and voiding/filling (V-F) dysfunction. Indeed, we currently
lack a full 3D biomechanical model for the whole bladder V-F process for even healthy bladders, let alone for
the BOO bladder as it goes through progressive changes over time scales of weeks and months. Our limited
understanding of bladder biomechanics is in sharp contrast to our knowledge of heart biomechanics, for which
sophisticated multi-scale, multi-physics models of the cyclic filling and emptying of the heart chambers have
been developed to understand cardiac disease and design patient specific treatments. Promisingly, there is
opportunity to capitalize on tools and experimental/computational approaches developed for other organs,
such as the heart, to rapidly advance the bladder biomechanics research field towards clinical impact.
To address this need, this R01 project will make use of state of the art in vivo and in vitro studies of BOO in a
rat model to drive the development of a digital twin of the whole BOO bladder. This data and the in silico
model will enable a mechanistic understanding of how changes to the BOO bladder cause progressive bladder
dysfunction and how this dysfunction can be ameliorated through reversal surgery and pharmacological
treatment. The focus of Aim 1 is dysfunction in the V-F process. A 3D finite element model of urodynamics
coupled with data from the BOO rat model will be used to determine how changes to the bladder drive
dysfunction in the V-F cycle, at each stage of BOO. In Aim 2, we will determine how pharmacological treatment
can be used to ameliorate bladder dysfunction. Progressive changes to bladder wall will be modeled over a
time scale of weeks using our computational framework for BOO mechanobiology. In Aim 3, we will use animal
data and the digital twin to determine mechanistic causes for bladder response to reversal surgery and identify
conditions for functional recovery with regards to surgical timing and pharmacological intervent...

## Key facts

- **NIH application ID:** 10906179
- **Project number:** 5R01DK133434-02
- **Recipient organization:** UNIVERSITY OF PITTSBURGH AT PITTSBURGH
- **Principal Investigator:** Anne Marie Robertson
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $614,430
- **Award type:** 5
- **Project period:** 2023-08-11 → 2028-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10906179

## Citation

> US National Institutes of Health, RePORTER application 10906179, A Digital Twin for Designing Bladder Treatment informed by Bladder Outlet Obstruction Mechanobiology (BOOM) (5R01DK133434-02). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10906179. Licensed CC0.

---

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